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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Long Non-Coding RNA: Dual Effects on Breast Cancer Metastasis and Clinical Applications</title><author><name sortKey="Huang, Qi Yuan" sort="Huang, Qi Yuan" uniqKey="Huang Q" first="Qi-Yuan" last="Huang">Qi-Yuan Huang</name><affiliation><nlm:aff id="af1-cancers-11-01802">Department of Pathophysiology, Basic Medical College, Nanchang University, Nanchang 330006, China;<email>6301616056@email.ncu.edu.cn</email> (Q.-Y.H.);<email>6302615051@email.ncu.edu.cn</email> (X.-L.Q.);<email>lb525912836@163.com</email> (L.-B.T.);<email>401442718029@email.ncu.edu.cn</email> (Q.-Y.H.)</nlm:aff></affiliation><affiliation><nlm:aff id="af2-cancers-11-01802">Second Clinical Medical College, Nanchang University, Nanchang 330006, China</nlm:aff></affiliation></author><author><name sortKey="Liu, Guo Feng" sort="Liu, Guo Feng" uniqKey="Liu G" first="Guo-Feng" last="Liu">Guo-Feng Liu</name><affiliation><nlm:aff id="af3-cancers-11-01802">First Clinical Medical College, Nanchang University, Nanchang 330006, China;<email>6302615053@email.ncu.edu.cn</email></nlm:aff></affiliation></author><author><name sortKey="Qian, Xian Ling" sort="Qian, Xian Ling" uniqKey="Qian X" first="Xian-Ling" last="Qian">Xian-Ling Qian</name><affiliation><nlm:aff id="af1-cancers-11-01802">Department of Pathophysiology, Basic Medical College, Nanchang University, Nanchang 330006, China;<email>6301616056@email.ncu.edu.cn</email> (Q.-Y.H.);<email>6302615051@email.ncu.edu.cn</email> (X.-L.Q.);<email>lb525912836@163.com</email> (L.-B.T.);<email>401442718029@email.ncu.edu.cn</email> (Q.-Y.H.)</nlm:aff></affiliation><affiliation><nlm:aff id="af3-cancers-11-01802">First Clinical Medical College, Nanchang University, Nanchang 330006, China;<email>6302615053@email.ncu.edu.cn</email></nlm:aff></affiliation></author><author><name sortKey="Tang, Li Bo" sort="Tang, Li Bo" uniqKey="Tang L" first="Li-Bo" last="Tang">Li-Bo Tang</name><affiliation><nlm:aff id="af1-cancers-11-01802">Department of Pathophysiology, Basic Medical College, Nanchang University, Nanchang 330006, China;<email>6301616056@email.ncu.edu.cn</email> (Q.-Y.H.);<email>6302615051@email.ncu.edu.cn</email> (X.-L.Q.);<email>lb525912836@163.com</email> (L.-B.T.);<email>401442718029@email.ncu.edu.cn</email> (Q.-Y.H.)</nlm:aff></affiliation><affiliation><nlm:aff id="af2-cancers-11-01802">Second Clinical Medical College, Nanchang University, Nanchang 330006, China</nlm:aff></affiliation></author><author><name sortKey="Huang, Qing Yun" sort="Huang, Qing Yun" uniqKey="Huang Q" first="Qing-Yun" last="Huang">Qing-Yun Huang</name><affiliation><nlm:aff id="af1-cancers-11-01802">Department of Pathophysiology, Basic Medical College, Nanchang University, Nanchang 330006, China;<email>6301616056@email.ncu.edu.cn</email> (Q.-Y.H.);<email>6302615051@email.ncu.edu.cn</email> (X.-L.Q.);<email>lb525912836@163.com</email> (L.-B.T.);<email>401442718029@email.ncu.edu.cn</email> (Q.-Y.H.)</nlm:aff></affiliation></author><author><name sortKey="Xiong, Li Xia" sort="Xiong, Li Xia" uniqKey="Xiong L" first="Li-Xia" last="Xiong">Li-Xia Xiong</name><affiliation><nlm:aff id="af1-cancers-11-01802">Department of Pathophysiology, Basic Medical College, Nanchang University, Nanchang 330006, China;<email>6301616056@email.ncu.edu.cn</email> (Q.-Y.H.);<email>6302615051@email.ncu.edu.cn</email> (X.-L.Q.);<email>lb525912836@163.com</email> (L.-B.T.);<email>401442718029@email.ncu.edu.cn</email> (Q.-Y.H.)</nlm:aff></affiliation><affiliation><nlm:aff id="af4-cancers-11-01802">Jiangxi Province Key Laboratory of Tumor Pathogenesis and Molecular Pathology, Nanchang 330006, China</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31744046</idno><idno type="pmc">6896003</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6896003</idno><idno type="RBID">PMC:6896003</idno><idno type="doi">10.3390/cancers11111802</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000906</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000906</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Long Non-Coding RNA: Dual Effects on Breast Cancer Metastasis and Clinical Applications</title><author><name sortKey="Huang, Qi Yuan" sort="Huang, Qi Yuan" uniqKey="Huang Q" first="Qi-Yuan" last="Huang">Qi-Yuan Huang</name><affiliation><nlm:aff id="af1-cancers-11-01802">Department of Pathophysiology, Basic Medical College, Nanchang University, Nanchang 330006, China;<email>6301616056@email.ncu.edu.cn</email> (Q.-Y.H.);<email>6302615051@email.ncu.edu.cn</email> (X.-L.Q.);<email>lb525912836@163.com</email> (L.-B.T.);<email>401442718029@email.ncu.edu.cn</email> (Q.-Y.H.)</nlm:aff></affiliation><affiliation><nlm:aff id="af2-cancers-11-01802">Second Clinical Medical College, Nanchang University, Nanchang 330006, China</nlm:aff></affiliation></author><author><name sortKey="Liu, Guo Feng" sort="Liu, Guo Feng" uniqKey="Liu G" first="Guo-Feng" last="Liu">Guo-Feng Liu</name><affiliation><nlm:aff id="af3-cancers-11-01802">First Clinical Medical College, Nanchang University, Nanchang 330006, China;<email>6302615053@email.ncu.edu.cn</email></nlm:aff></affiliation></author><author><name sortKey="Qian, Xian Ling" sort="Qian, Xian Ling" uniqKey="Qian X" first="Xian-Ling" last="Qian">Xian-Ling Qian</name><affiliation><nlm:aff id="af1-cancers-11-01802">Department of Pathophysiology, Basic Medical College, Nanchang University, Nanchang 330006, China;<email>6301616056@email.ncu.edu.cn</email> (Q.-Y.H.);<email>6302615051@email.ncu.edu.cn</email> (X.-L.Q.);<email>lb525912836@163.com</email> (L.-B.T.);<email>401442718029@email.ncu.edu.cn</email> (Q.-Y.H.)</nlm:aff></affiliation><affiliation><nlm:aff id="af3-cancers-11-01802">First Clinical Medical College, Nanchang University, Nanchang 330006, China;<email>6302615053@email.ncu.edu.cn</email></nlm:aff></affiliation></author><author><name sortKey="Tang, Li Bo" sort="Tang, Li Bo" uniqKey="Tang L" first="Li-Bo" last="Tang">Li-Bo Tang</name><affiliation><nlm:aff id="af1-cancers-11-01802">Department of Pathophysiology, Basic Medical College, Nanchang University, Nanchang 330006, China;<email>6301616056@email.ncu.edu.cn</email> (Q.-Y.H.);<email>6302615051@email.ncu.edu.cn</email> (X.-L.Q.);<email>lb525912836@163.com</email> (L.-B.T.);<email>401442718029@email.ncu.edu.cn</email> (Q.-Y.H.)</nlm:aff></affiliation><affiliation><nlm:aff id="af2-cancers-11-01802">Second Clinical Medical College, Nanchang University, Nanchang 330006, China</nlm:aff></affiliation></author><author><name sortKey="Huang, Qing Yun" sort="Huang, Qing Yun" uniqKey="Huang Q" first="Qing-Yun" last="Huang">Qing-Yun Huang</name><affiliation><nlm:aff id="af1-cancers-11-01802">Department of Pathophysiology, Basic Medical College, Nanchang University, Nanchang 330006, China;<email>6301616056@email.ncu.edu.cn</email> (Q.-Y.H.);<email>6302615051@email.ncu.edu.cn</email> (X.-L.Q.);<email>lb525912836@163.com</email> (L.-B.T.);<email>401442718029@email.ncu.edu.cn</email> (Q.-Y.H.)</nlm:aff></affiliation></author><author><name sortKey="Xiong, Li Xia" sort="Xiong, Li Xia" uniqKey="Xiong L" first="Li-Xia" last="Xiong">Li-Xia Xiong</name><affiliation><nlm:aff id="af1-cancers-11-01802">Department of Pathophysiology, Basic Medical College, Nanchang University, Nanchang 330006, China;<email>6301616056@email.ncu.edu.cn</email> (Q.-Y.H.);<email>6302615051@email.ncu.edu.cn</email> (X.-L.Q.);<email>lb525912836@163.com</email> (L.-B.T.);<email>401442718029@email.ncu.edu.cn</email> (Q.-Y.H.)</nlm:aff></affiliation><affiliation><nlm:aff id="af4-cancers-11-01802">Jiangxi Province Key Laboratory of Tumor Pathogenesis and Molecular Pathology, Nanchang 330006, China</nlm:aff></affiliation></author></analytic><series><title level="j">Cancers</title><idno type="eISSN">2072-6694</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>As a highly heterogeneous malignancy, breast cancer (BC) has become the most significant threat to female health. Distant metastasis and therapy resistance of BC are responsible for most of the cases of mortality and recurrence. Distant metastasis relies on an array of processes, such as cell proliferation, epithelial-to-mesenchymal transition (EMT), mesenchymal-to-epithelial transition (MET), and angiogenesis. Long non-coding RNA (lncRNA) refers to a class of non-coding RNA with a length of over 200 nucleotides. Currently, a rising number of studies have managed to investigate the association between BC and lncRNA. In this study, we summarized how lncRNA has dual effects in BC metastasis by regulating invasion, migration, and distant metastasis of BC cells. We also emphasize that lncRNA has crucial regulatory effects in the stemness and angiogenesis of BC. Clinically, some lncRNAs can regulate chemotherapy sensitivity in BC patients and may function as novel biomarkers to diagnose or predict prognosis for BC patients. The exact impact on clinical relevance deserves further study. This review can be an approach to understanding the dual effects of lncRNAs in BC, thereby linking lncRNAs to quasi-personalized treatment in the future.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Bray, F" uniqKey="Bray F">F. Bray</name></author><author><name sortKey="Ferlay, J" uniqKey="Ferlay J">J. Ferlay</name></author><author><name sortKey="Soerjomataram, I" uniqKey="Soerjomataram I">I. Soerjomataram</name></author><author><name sortKey="Siegel, R" uniqKey="Siegel R">R. Siegel</name></author><author><name sortKey="Torre, L" uniqKey="Torre L">L. Torre</name></author><author><name sortKey="Jemal, A" uniqKey="Jemal A">A. Jemal</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ponde, N" uniqKey="Ponde N">N. Pondé</name></author><author><name sortKey="Brandao, M" uniqKey="Brandao M">M. Brandão</name></author><author><name sortKey="El Hachem, G" uniqKey="El Hachem G">G. El-Hachem</name></author><author><name sortKey="Werbrouck, E" uniqKey="Werbrouck E">E. Werbrouck</name></author><author><name sortKey="Piccart, M" uniqKey="Piccart M">M. Piccart</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Suba, Z" uniqKey="Suba Z">Z. Suba</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gadi, V K" uniqKey="Gadi V">V.K. Gadi</name></author><author><name sortKey="Davidson, N E" uniqKey="Davidson N">N.E. Davidson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rabanal, C" uniqKey="Rabanal C">C. Rabanal</name></author><author><name sortKey="Ruiz, R" uniqKey="Ruiz R">R. Ruiz</name></author><author><name sortKey="Neciosup, S" uniqKey="Neciosup S">S. Neciosup</name></author><author><name sortKey="Gomez, H" uniqKey="Gomez H">H. Gomez</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pastushenko, I" uniqKey="Pastushenko I">I. Pastushenko</name></author><author><name sortKey="Brisebarre, A" uniqKey="Brisebarre A">A. Brisebarre</name></author><author><name sortKey="Sifrim, A" uniqKey="Sifrim A">A. Sifrim</name></author><author><name sortKey="Fioramonti, M" uniqKey="Fioramonti M">M. Fioramonti</name></author><author><name sortKey="Revenco, T" uniqKey="Revenco T">T. Revenco</name></author><author><name sortKey="Boumahdi, S" uniqKey="Boumahdi S">S. Boumahdi</name></author><author><name sortKey="Van Keymeulen, A" uniqKey="Van Keymeulen A">A. Van Keymeulen</name></author><author><name sortKey="Brown, D" uniqKey="Brown D">D. Brown</name></author><author><name sortKey="Moers, V" uniqKey="Moers V">V. Moers</name></author><author><name sortKey="Lemaire, S" uniqKey="Lemaire S">S. Lemaire</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mitra, A" uniqKey="Mitra A">A. Mitra</name></author><author><name sortKey="Mishra, L" uniqKey="Mishra L">L. Mishra</name></author><author><name sortKey="Li, S" uniqKey="Li S">S. Li</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Morris, K V" uniqKey="Morris K">K.V. Morris</name></author><author><name sortKey="Mattick, J S" uniqKey="Mattick J">J.S. Mattick</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ponting, C P" uniqKey="Ponting C">C.P. Ponting</name></author><author><name sortKey="Oliver, P L" uniqKey="Oliver P">P.L. Oliver</name></author><author><name sortKey="Reik, W" uniqKey="Reik W">W. Reik</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Evans, J R" uniqKey="Evans J">J.R. Evans</name></author><author><name sortKey="Feng, F Y" uniqKey="Feng F">F.Y. Feng</name></author><author><name sortKey="Chinnaiyan, A M" uniqKey="Chinnaiyan A">A.M. Chinnaiyan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Congrains, A" uniqKey="Congrains A">A. Congrains</name></author><author><name sortKey="Kamide, K" uniqKey="Kamide K">K. Kamide</name></author><author><name sortKey="Oguro, R" uniqKey="Oguro R">R. Oguro</name></author><author><name sortKey="Yasuda, O" uniqKey="Yasuda O">O. Yasuda</name></author><author><name sortKey="Miyata, K" uniqKey="Miyata K">K. Miyata</name></author><author><name sortKey="Yamamoto, E" uniqKey="Yamamoto E">E. Yamamoto</name></author><author><name sortKey="Kawai, T" uniqKey="Kawai T">T. Kawai</name></author><author><name sortKey="Kusunoki, H" uniqKey="Kusunoki H">H. Kusunoki</name></author><author><name sortKey="Yamamoto, H" uniqKey="Yamamoto H">H. Yamamoto</name></author><author><name sortKey="Takeya, Y" uniqKey="Takeya Y">Y. Takeya</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, Y" uniqKey="Yang Y">Y. Yang</name></author><author><name sortKey="Cai, Y" uniqKey="Cai Y">Y. Cai</name></author><author><name sortKey="Wu, G" uniqKey="Wu G">G. Wu</name></author><author><name sortKey="Chen, X" uniqKey="Chen X">X. Chen</name></author><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Yu, J" uniqKey="Yu J">J. Yu</name></author><author><name sortKey="Li, C" uniqKey="Li C">C. Li</name></author><author><name sortKey="Chen, X" uniqKey="Chen X">X. Chen</name></author><author><name sortKey="Jose, P" uniqKey="Jose P">P. Jose</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ashraf, G" uniqKey="Ashraf G">G. Ashraf</name></author><author><name sortKey="Ganash, M" uniqKey="Ganash M">M. Ganash</name></author><author><name sortKey="Athanasios, A" uniqKey="Athanasios A">A. Athanasios</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Huang, X" uniqKey="Huang X">X. Huang</name></author><author><name sortKey="Luo, Y L" uniqKey="Luo Y">Y.L. Luo</name></author><author><name sortKey="Mao, Y S" uniqKey="Mao Y">Y.S. Mao</name></author><author><name sortKey="Ji, J L" uniqKey="Ji J">J.L. Ji</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mirza, A H" uniqKey="Mirza A">A.H. Mirza</name></author><author><name sortKey="Kaur, S" uniqKey="Kaur S">S. Kaur</name></author><author><name sortKey="Pociot, F" uniqKey="Pociot F">F. Pociot</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lorenzi, L" uniqKey="Lorenzi L">L. Lorenzi</name></author><author><name sortKey="Avila Cobos, F" uniqKey="Avila Cobos F">F. Avila Cobos</name></author><author><name sortKey="Decock, A" uniqKey="Decock A">A. Decock</name></author><author><name sortKey="Everaert, C" uniqKey="Everaert C">C. Everaert</name></author><author><name sortKey="Helsmoortel, H" uniqKey="Helsmoortel H">H. Helsmoortel</name></author><author><name sortKey="Lefever, S" uniqKey="Lefever S">S. Lefever</name></author><author><name sortKey="Verboom, K" uniqKey="Verboom K">K. Verboom</name></author><author><name sortKey="Volders, P" uniqKey="Volders P">P. Volders</name></author><author><name sortKey="Speleman, F" uniqKey="Speleman F">F. Speleman</name></author><author><name sortKey="Vandesompele, J" uniqKey="Vandesompele J">J. Vandesompele</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Angrand, P" uniqKey="Angrand P">P. Angrand</name></author><author><name sortKey="Vennin, C" uniqKey="Vennin C">C. Vennin</name></author><author><name sortKey="Le Bourhis, X" uniqKey="Le Bourhis X">X. Le Bourhis</name></author><author><name sortKey="Adriaenssens, E" uniqKey="Adriaenssens E">E. Adriaenssens</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fan, C" uniqKey="Fan C">C. Fan</name></author><author><name sortKey="Ma, L" uniqKey="Ma L">L. Ma</name></author><author><name sortKey="Liu, N" uniqKey="Liu N">N. Liu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Huang, Y" uniqKey="Huang Y">Y. Huang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lian, Y" uniqKey="Lian Y">Y. Lian</name></author><author><name sortKey="Xiong, F" uniqKey="Xiong F">F. Xiong</name></author><author><name sortKey="Yang, L" uniqKey="Yang L">L. Yang</name></author><author><name sortKey="Bo, H" uniqKey="Bo H">H. Bo</name></author><author><name sortKey="Gong, Z" uniqKey="Gong Z">Z. Gong</name></author><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y. Wang</name></author><author><name sortKey="Wei, F" uniqKey="Wei F">F. Wei</name></author><author><name sortKey="Tang, Y" uniqKey="Tang Y">Y. Tang</name></author><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author><author><name sortKey="Liao, Q" uniqKey="Liao Q">Q. Liao</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, X" uniqKey="Yang X">X. Yang</name></author><author><name sortKey="Cheng, T" uniqKey="Cheng T">T. Cheng</name></author><author><name sortKey="He, Q" uniqKey="He Q">Q. He</name></author><author><name sortKey="Lei, Z" uniqKey="Lei Z">Z. Lei</name></author><author><name sortKey="Chi, J" uniqKey="Chi J">J. Chi</name></author><author><name sortKey="Tang, Z" uniqKey="Tang Z">Z. Tang</name></author><author><name sortKey="Liao, Q" uniqKey="Liao Q">Q. Liao</name></author><author><name sortKey="Zhang, H" uniqKey="Zhang H">H. Zhang</name></author><author><name sortKey="Zeng, L" uniqKey="Zeng L">L. Zeng</name></author><author><name sortKey="Cui, S" uniqKey="Cui S">S. Cui</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Leucci, E" uniqKey="Leucci E">E. Leucci</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yuan, S" uniqKey="Yuan S">S. Yuan</name></author><author><name sortKey="Wang, J" uniqKey="Wang J">J. Wang</name></author><author><name sortKey="Yang, F" uniqKey="Yang F">F. Yang</name></author><author><name sortKey="Tao, Q" uniqKey="Tao Q">Q. Tao</name></author><author><name sortKey="Zhang, J" uniqKey="Zhang J">J. Zhang</name></author><author><name sortKey="Wang, L" uniqKey="Wang L">L. Wang</name></author><author><name sortKey="Yang, Y" uniqKey="Yang Y">Y. Yang</name></author><author><name sortKey="Liu, H" uniqKey="Liu H">H. Liu</name></author><author><name sortKey="Wang, Z" uniqKey="Wang Z">Z. Wang</name></author><author><name sortKey="Xu, Q" uniqKey="Xu Q">Q. Xu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author><author><name sortKey="Zhang, M" uniqKey="Zhang M">M. Zhang</name></author><author><name sortKey="Liang, L" uniqKey="Liang L">L. Liang</name></author><author><name sortKey="Li, J" uniqKey="Li J">J. Li</name></author><author><name sortKey="Chen, Y" uniqKey="Chen Y">Y. Chen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sha, S" uniqKey="Sha S">S. Sha</name></author><author><name sortKey="Yuan, D" uniqKey="Yuan D">D. Yuan</name></author><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author><author><name sortKey="Han, B" uniqKey="Han B">B. Han</name></author><author><name sortKey="Zhong, N" uniqKey="Zhong N">N. Zhong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hock, H" uniqKey="Hock H">H. Hock</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Vaidya, A M" uniqKey="Vaidya A">A.M. Vaidya</name></author><author><name sortKey="Sun, Z" uniqKey="Sun Z">Z. Sun</name></author><author><name sortKey="Ayat, N" uniqKey="Ayat N">N. Ayat</name></author><author><name sortKey="Schilb, A" uniqKey="Schilb A">A. Schilb</name></author><author><name sortKey="Liu, X" uniqKey="Liu X">X. Liu</name></author><author><name sortKey="Jiang, H" uniqKey="Jiang H">H. Jiang</name></author><author><name sortKey="Sun, D" uniqKey="Sun D">D. Sun</name></author><author><name sortKey="Scheidt, J" uniqKey="Scheidt J">J. Scheidt</name></author><author><name sortKey="Qian, V" uniqKey="Qian V">V. Qian</name></author><author><name sortKey="He, S" uniqKey="He S">S. He</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tao, W" uniqKey="Tao W">W. Tao</name></author><author><name sortKey="Wang, C" uniqKey="Wang C">C. Wang</name></author><author><name sortKey="Zhu, B" uniqKey="Zhu B">B. Zhu</name></author><author><name sortKey="Zhang, G" uniqKey="Zhang G">G. Zhang</name></author><author><name sortKey="Pang, D" uniqKey="Pang D">D. Pang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Muller, V" uniqKey="Muller V">V. Muller</name></author><author><name sortKey="Ferrer, L O" uniqKey="Ferrer L">L.O. Ferrer</name></author><author><name sortKey="Steinbach, B" uniqKey="Steinbach B">B. Steinbach</name></author><author><name sortKey="Pantel, K" uniqKey="Pantel K">K. Pantel</name></author><author><name sortKey="Schwarzenbach, H" uniqKey="Schwarzenbach H">H. Schwarzenbach</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lottin, S" uniqKey="Lottin S">S. Lottin</name></author><author><name sortKey="Adriaenssens, E" uniqKey="Adriaenssens E">E. Adriaenssens</name></author><author><name sortKey="Dupressoir, T" uniqKey="Dupressoir T">T. Dupressoir</name></author><author><name sortKey="Berteaux, N" uniqKey="Berteaux N">N. Berteaux</name></author><author><name sortKey="Montpellier, C" uniqKey="Montpellier C">C. Montpellier</name></author><author><name sortKey="Coll, J" uniqKey="Coll J">J. Coll</name></author><author><name sortKey="Dugimont, T" uniqKey="Dugimont T">T. Dugimont</name></author><author><name sortKey="Curgy, J J" uniqKey="Curgy J">J.J. Curgy</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kastl, L" uniqKey="Kastl L">L. Kastl</name></author><author><name sortKey="Brown, I" uniqKey="Brown I">I. Brown</name></author><author><name sortKey="Schofield, A C" uniqKey="Schofield A">A.C. Schofield</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rajabi, H" uniqKey="Rajabi H">H. Rajabi</name></author><author><name sortKey="Tagde, A" uniqKey="Tagde A">A. Tagde</name></author><author><name sortKey="Alam, M" uniqKey="Alam M">M. Alam</name></author><author><name sortKey="Bouillez, A" uniqKey="Bouillez A">A. Bouillez</name></author><author><name sortKey="Pitroda, S" uniqKey="Pitroda S">S. Pitroda</name></author><author><name sortKey="Suzuki, Y" uniqKey="Suzuki Y">Y. Suzuki</name></author><author><name sortKey="Kufe, D" uniqKey="Kufe D">D. Kufe</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, W" uniqKey="Zhang W">W. Zhang</name></author><author><name sortKey="Chang, Z" uniqKey="Chang Z">Z. Chang</name></author><author><name sortKey="Shi, K E" uniqKey="Shi K">K.E. Shi</name></author><author><name sortKey="Song, L" uniqKey="Song L">L. Song</name></author><author><name sortKey="Cui, L I" uniqKey="Cui L">L.I. Cui</name></author><author><name sortKey="Ma, Z" uniqKey="Ma Z">Z. Ma</name></author><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author><author><name sortKey="Ma, W" uniqKey="Ma W">W. Ma</name></author><author><name sortKey="Wang, L" uniqKey="Wang L">L. Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, Z" uniqKey="Li Z">Z. Li</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y. Li</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y. Li</name></author><author><name sortKey="Ren, K" uniqKey="Ren K">K. Ren</name></author><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author><author><name sortKey="Han, X" uniqKey="Han X">X. Han</name></author><author><name sortKey="Wang, J" uniqKey="Wang J">J. Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bates, P" uniqKey="Bates P">P. Bates</name></author><author><name sortKey="Fisher, R" uniqKey="Fisher R">R. Fisher</name></author><author><name sortKey="Ward, A" uniqKey="Ward A">A. Ward</name></author><author><name sortKey="Richardson, L" uniqKey="Richardson L">L. Richardson</name></author><author><name sortKey="Hill, D J" uniqKey="Hill D">D.J. Hill</name></author><author><name sortKey="Graham, C F" uniqKey="Graham C">C.F. Graham</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Min, H" uniqKey="Min H">H. Min</name></author><author><name sortKey="Lee, S" uniqKey="Lee S">S. Lee</name></author><author><name sortKey="Woo, J" uniqKey="Woo J">J. Woo</name></author><author><name sortKey="Jung, H" uniqKey="Jung H">H. Jung</name></author><author><name sortKey="Park, K" uniqKey="Park K">K. Park</name></author><author><name sortKey="Jeong, H" uniqKey="Jeong H">H. Jeong</name></author><author><name sortKey="Hyun, S" uniqKey="Hyun S">S. Hyun</name></author><author><name sortKey="Cho, J" uniqKey="Cho J">J. Cho</name></author><author><name sortKey="Lee, W" uniqKey="Lee W">W. Lee</name></author><author><name sortKey="Park, J" uniqKey="Park J">J. Park</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Vennin, C" uniqKey="Vennin C">C. Vennin</name></author><author><name sortKey="Spruyt, N" uniqKey="Spruyt N">N. Spruyt</name></author><author><name sortKey="Robin, Y M" uniqKey="Robin Y">Y.M. Robin</name></author><author><name sortKey="Chassat, T" uniqKey="Chassat T">T. Chassat</name></author><author><name sortKey="Le Bourhis, X" uniqKey="Le Bourhis X">X. Le Bourhis</name></author><author><name sortKey="Adriaenssens, E" uniqKey="Adriaenssens E">E. Adriaenssens</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tran, V" uniqKey="Tran V">V. Tran</name></author><author><name sortKey="Court, F" uniqKey="Court F">F. Court</name></author><author><name sortKey="Duputie, A" uniqKey="Duputie A">A. Duputié</name></author><author><name sortKey="Antoine, E" uniqKey="Antoine E">E. Antoine</name></author><author><name sortKey="Aptel, N" uniqKey="Aptel N">N. Aptel</name></author><author><name sortKey="Milligan, L" uniqKey="Milligan L">L. Milligan</name></author><author><name sortKey="Carbonell, F" uniqKey="Carbonell F">F. Carbonell</name></author><author><name sortKey="Lelay Taha, M" uniqKey="Lelay Taha M">M. Lelay-Taha</name></author><author><name sortKey="Piette, J" uniqKey="Piette J">J. Piette</name></author><author><name sortKey="Weber, M" uniqKey="Weber M">M. Weber</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="S Rensen, K" uniqKey="S Rensen K">K. Sørensen</name></author><author><name sortKey="Thomassen, M" uniqKey="Thomassen M">M. Thomassen</name></author><author><name sortKey="Tan, Q" uniqKey="Tan Q">Q. Tan</name></author><author><name sortKey="Bak, M" uniqKey="Bak M">M. Bak</name></author><author><name sortKey="Cold, S" uniqKey="Cold S">S. Cold</name></author><author><name sortKey="Burton, M" uniqKey="Burton M">M. Burton</name></author><author><name sortKey="Larsen, M" uniqKey="Larsen M">M. Larsen</name></author><author><name sortKey="Kruse, T" uniqKey="Kruse T">T. Kruse</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhuang, Y" uniqKey="Zhuang Y">Y. Zhuang</name></author><author><name sortKey="Nguyen, H" uniqKey="Nguyen H">H. Nguyen</name></author><author><name sortKey="Burow, M" uniqKey="Burow M">M. Burow</name></author><author><name sortKey="Zhuo, Y" uniqKey="Zhuo Y">Y. Zhuo</name></author><author><name sortKey="El Dahr, S" uniqKey="El Dahr S">S. El-Dahr</name></author><author><name sortKey="Yao, X" uniqKey="Yao X">X. Yao</name></author><author><name sortKey="Cao, S" uniqKey="Cao S">S. Cao</name></author><author><name sortKey="Flemington, E" uniqKey="Flemington E">E. Flemington</name></author><author><name sortKey="Nephew, K" uniqKey="Nephew K">K. Nephew</name></author><author><name sortKey="Fang, F" uniqKey="Fang F">F. Fang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kim, H J" uniqKey="Kim H">H.J. Kim</name></author><author><name sortKey="Lee, D W" uniqKey="Lee D">D.W. Lee</name></author><author><name sortKey="Yim, G W" uniqKey="Yim G">G.W. Yim</name></author><author><name sortKey="Nam, E J" uniqKey="Nam E">E.J. Nam</name></author><author><name sortKey="Kim, S" uniqKey="Kim S">S. Kim</name></author><author><name sortKey="Kim, S W" uniqKey="Kim S">S.W. Kim</name></author><author><name sortKey="Kim, Y T" uniqKey="Kim Y">Y.T. Kim</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yu, Y" uniqKey="Yu Y">Y. Yu</name></author><author><name sortKey="Lv, F" uniqKey="Lv F">F. Lv</name></author><author><name sortKey="Liang, D" uniqKey="Liang D">D. Liang</name></author><author><name sortKey="Yang, Q" uniqKey="Yang Q">Q. Yang</name></author><author><name sortKey="Zhang, B" uniqKey="Zhang B">B. Zhang</name></author><author><name sortKey="Lin, H" uniqKey="Lin H">H. Lin</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Qian, G" uniqKey="Qian G">G. Qian</name></author><author><name sortKey="Xu, J" uniqKey="Xu J">J. Xu</name></author><author><name sortKey="You, W" uniqKey="You W">W. You</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Huang, Y" uniqKey="Huang Y">Y. Huang</name></author><author><name sortKey="Du, J" uniqKey="Du J">J. Du</name></author><author><name sortKey="Mi, Y" uniqKey="Mi Y">Y. Mi</name></author><author><name sortKey="Li, T" uniqKey="Li T">T. Li</name></author><author><name sortKey="Gong, Y" uniqKey="Gong Y">Y. Gong</name></author><author><name sortKey="Ouyang, H" uniqKey="Ouyang H">H. Ouyang</name></author><author><name sortKey="Hou, Y" uniqKey="Hou Y">Y. Hou</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhao, W" uniqKey="Zhao W">W. Zhao</name></author><author><name sortKey="Geng, D" uniqKey="Geng D">D. Geng</name></author><author><name sortKey="Li, S" uniqKey="Li S">S. Li</name></author><author><name sortKey="Chen, Z" uniqKey="Chen Z">Z. Chen</name></author><author><name sortKey="Sun, M" uniqKey="Sun M">M. Sun</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cogill, S B" uniqKey="Cogill S">S.B. Cogill</name></author><author><name sortKey="Wang, L" uniqKey="Wang L">L. Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wu, J" uniqKey="Wu J">J. Wu</name></author><author><name sortKey="Shuang, Z" uniqKey="Shuang Z">Z. Shuang</name></author><author><name sortKey="Zhao, J" uniqKey="Zhao J">J. Zhao</name></author><author><name sortKey="Tang, H" uniqKey="Tang H">H. Tang</name></author><author><name sortKey="Liu, P" uniqKey="Liu P">P. Liu</name></author><author><name sortKey="Zhang, L" uniqKey="Zhang L">L. Zhang</name></author><author><name sortKey="Xie, X" uniqKey="Xie X">X. Xie</name></author><author><name sortKey="Xiao, X" uniqKey="Xiao X">X. Xiao</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hu, X L" uniqKey="Hu X">X.L. Hu</name></author><author><name sortKey="Wang, J" uniqKey="Wang J">J. Wang</name></author><author><name sortKey="He, W" uniqKey="He W">W. He</name></author><author><name sortKey="Zhao, P" uniqKey="Zhao P">P. Zhao</name></author><author><name sortKey="Wu, W Q" uniqKey="Wu W">W.Q. Wu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xu, S" uniqKey="Xu S">S. Xu</name></author><author><name sortKey="Wan, L" uniqKey="Wan L">L. Wan</name></author><author><name sortKey="Yin, H" uniqKey="Yin H">H. Yin</name></author><author><name sortKey="Xu, H" uniqKey="Xu H">H. Xu</name></author><author><name sortKey="Zheng, W" uniqKey="Zheng W">W. Zheng</name></author><author><name sortKey="Shen, M" uniqKey="Shen M">M. Shen</name></author><author><name sortKey="Zhang, Z" uniqKey="Zhang Z">Z. Zhang</name></author><author><name sortKey="Pang, D" uniqKey="Pang D">D. Pang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, Y" uniqKey="Yang Y">Y. Yang</name></author><author><name sortKey="Ren, M" uniqKey="Ren M">M. Ren</name></author><author><name sortKey="Song, C" uniqKey="Song C">C. Song</name></author><author><name sortKey="Li, D" uniqKey="Li D">D. Li</name></author><author><name sortKey="Soomro, S H" uniqKey="Soomro S">S.H. Soomro</name></author><author><name sortKey="Xiong, Y" uniqKey="Xiong Y">Y. Xiong</name></author><author><name sortKey="Zhang, H" uniqKey="Zhang H">H. Zhang</name></author><author><name sortKey="Fu, H" uniqKey="Fu H">H. Fu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shim, H S" uniqKey="Shim H">H.S. Shim</name></author><author><name sortKey="Yoon, B S" uniqKey="Yoon B">B.S. Yoon</name></author><author><name sortKey="Cho, N H" uniqKey="Cho N">N.H. Cho</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dong, L" uniqKey="Dong L">L. Dong</name></author><author><name sortKey="Qian, J" uniqKey="Qian J">J. Qian</name></author><author><name sortKey="Chen, F" uniqKey="Chen F">F. Chen</name></author><author><name sortKey="Fan, Y" uniqKey="Fan Y">Y. Fan</name></author><author><name sortKey="Long, J" uniqKey="Long J">J. Long</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Murakami, A" uniqKey="Murakami A">A. Murakami</name></author><author><name sortKey="Nakagawa, T" uniqKey="Nakagawa T">T. Nakagawa</name></author><author><name sortKey="Fukushima, C" uniqKey="Fukushima C">C. Fukushima</name></author><author><name sortKey="Torii, M" uniqKey="Torii M">M. Torii</name></author><author><name sortKey="Sueoka, K" uniqKey="Sueoka K">K. Sueoka</name></author><author><name sortKey="Nawata, S" uniqKey="Nawata S">S. Nawata</name></author><author><name sortKey="Takeda, O" uniqKey="Takeda O">O. Takeda</name></author><author><name sortKey="Ishikawa, H" uniqKey="Ishikawa H">H. Ishikawa</name></author><author><name sortKey="Sugino, N" uniqKey="Sugino N">N. Sugino</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shi, Y" uniqKey="Shi Y">Y. Shi</name></author><author><name sortKey="Ye, P" uniqKey="Ye P">P. Ye</name></author><author><name sortKey="Long, X" uniqKey="Long X">X. Long</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jia, Y" uniqKey="Jia Y">Y. Jia</name></author><author><name sortKey="Shi, L" uniqKey="Shi L">L. Shi</name></author><author><name sortKey="Yun, F" uniqKey="Yun F">F. Yun</name></author><author><name sortKey="Liu, X" uniqKey="Liu X">X. Liu</name></author><author><name sortKey="Chen, Y" uniqKey="Chen Y">Y. Chen</name></author><author><name sortKey="Wang, M" uniqKey="Wang M">M. Wang</name></author><author><name sortKey="Chen, C" uniqKey="Chen C">C. Chen</name></author><author><name sortKey="Ren, Y" uniqKey="Ren Y">Y. Ren</name></author><author><name sortKey="Bao, Y" uniqKey="Bao Y">Y. Bao</name></author><author><name sortKey="Wang, L" uniqKey="Wang L">L. Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, M" uniqKey="Zhang M">M. Zhang</name></author><author><name sortKey="Wu, W B" uniqKey="Wu W">W.B. Wu</name></author><author><name sortKey="Wang, Z W" uniqKey="Wang Z">Z.W. Wang</name></author><author><name sortKey="Wang, X H" uniqKey="Wang X">X.H. Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jiang, X" uniqKey="Jiang X">X. Jiang</name></author><author><name sortKey="Zhou, Y" uniqKey="Zhou Y">Y. Zhou</name></author><author><name sortKey="Sun, A J" uniqKey="Sun A">A.J. Sun</name></author><author><name sortKey="Xue, J L" uniqKey="Xue J">J.L. Xue</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shin, V Y" uniqKey="Shin V">V.Y. Shin</name></author><author><name sortKey="Chen, J" uniqKey="Chen J">J. Chen</name></author><author><name sortKey="Cheuk, I W" uniqKey="Cheuk I">I.W. Cheuk</name></author><author><name sortKey="Siu, M T" uniqKey="Siu M">M.T. Siu</name></author><author><name sortKey="Ho, C W" uniqKey="Ho C">C.W. Ho</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Jin, H" uniqKey="Jin H">H. Jin</name></author><author><name sortKey="Kwong, A" uniqKey="Kwong A">A. Kwong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xiong, Y" uniqKey="Xiong Y">Y. Xiong</name></author><author><name sortKey="Gu, Y" uniqKey="Gu Y">Y. Gu</name></author><author><name sortKey="Wang, F" uniqKey="Wang F">F. Wang</name></author><author><name sortKey="Li, L" uniqKey="Li L">L. Li</name></author><author><name sortKey="Zhu, M" uniqKey="Zhu M">M. Zhu</name></author><author><name sortKey="Wang, N" uniqKey="Wang N">N. Wang</name></author><author><name sortKey="Mi, H" uniqKey="Mi H">H. Mi</name></author><author><name sortKey="Qiu, X" uniqKey="Qiu X">X. Qiu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jia, D" uniqKey="Jia D">D. Jia</name></author><author><name sortKey="Augert, A" uniqKey="Augert A">A. Augert</name></author><author><name sortKey="Kim, D" uniqKey="Kim D">D. Kim</name></author><author><name sortKey="Eastwood, E" uniqKey="Eastwood E">E. Eastwood</name></author><author><name sortKey="Wu, N" uniqKey="Wu N">N. Wu</name></author><author><name sortKey="Ibrahim, A" uniqKey="Ibrahim A">A. Ibrahim</name></author><author><name sortKey="Kim, K" uniqKey="Kim K">K. Kim</name></author><author><name sortKey="Dunn, C" uniqKey="Dunn C">C. Dunn</name></author><author><name sortKey="Pillai, S" uniqKey="Pillai S">S. Pillai</name></author><author><name sortKey="Gazdar, A" uniqKey="Gazdar A">A. Gazdar</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Garcia Carpizo, V" uniqKey="Garcia Carpizo V">V. Garcia-Carpizo</name></author><author><name sortKey="Ruiz Llorente, S" uniqKey="Ruiz Llorente S">S. Ruiz-Llorente</name></author><author><name sortKey="Sarmentero, J" uniqKey="Sarmentero J">J. Sarmentero</name></author><author><name sortKey="Gonzalez Corpas, A" uniqKey="Gonzalez Corpas A">A. González-Corpas</name></author><author><name sortKey="Barrero, M" uniqKey="Barrero M">M. Barrero</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhou, W" uniqKey="Zhou W">W. Zhou</name></author><author><name sortKey="Ye, X L" uniqKey="Ye X">X.L. Ye</name></author><author><name sortKey="Xu, J" uniqKey="Xu J">J. Xu</name></author><author><name sortKey="Cao, M G" uniqKey="Cao M">M.G. Cao</name></author><author><name sortKey="Fang, Z Y" uniqKey="Fang Z">Z.Y. Fang</name></author><author><name sortKey="Li, L Y" uniqKey="Li L">L.Y. Li</name></author><author><name sortKey="Guan, G H" uniqKey="Guan G">G.H. Guan</name></author><author><name sortKey="Liu, Q" uniqKey="Liu Q">Q. Liu</name></author><author><name sortKey="Qian, Y H" uniqKey="Qian Y">Y.H. Qian</name></author><author><name sortKey="Xie, D" uniqKey="Xie D">D. Xie</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Oca A, O" uniqKey="Oca A O">O. Ocaña</name></author><author><name sortKey="C Rcoles, R" uniqKey="C Rcoles R">R. Córcoles</name></author><author><name sortKey="Fabra, A" uniqKey="Fabra A">A. Fabra</name></author><author><name sortKey="Moreno Bueno, G" uniqKey="Moreno Bueno G">G. Moreno-Bueno</name></author><author><name sortKey="Acloque, H" uniqKey="Acloque H">H. Acloque</name></author><author><name sortKey="Vega, S" uniqKey="Vega S">S. Vega</name></author><author><name sortKey="Barrallo Gimeno, A" uniqKey="Barrallo Gimeno A">A. Barrallo-Gimeno</name></author><author><name sortKey="Cano, A" uniqKey="Cano A">A. Cano</name></author><author><name sortKey="Nieto, M" uniqKey="Nieto M">M. Nieto</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Beerling, E" uniqKey="Beerling E">E. Beerling</name></author><author><name sortKey="Seinstra, D" uniqKey="Seinstra D">D. Seinstra</name></author><author><name sortKey="De Wit, E" uniqKey="De Wit E">E. de Wit</name></author><author><name sortKey="Kester, L" uniqKey="Kester L">L. Kester</name></author><author><name sortKey="Van Der Velden, D" uniqKey="Van Der Velden D">D. van der Velden</name></author><author><name sortKey="Maynard, C" uniqKey="Maynard C">C. Maynard</name></author><author><name sortKey="Sch Fer, R" uniqKey="Sch Fer R">R. Schäfer</name></author><author><name sortKey="Van Diest, P" uniqKey="Van Diest P">P. van Diest</name></author><author><name sortKey="Voest, E" uniqKey="Voest E">E. Voest</name></author><author><name sortKey="Van Oudenaarden, A" uniqKey="Van Oudenaarden A">A. van Oudenaarden</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Matouk, I J" uniqKey="Matouk I">I.J. Matouk</name></author><author><name sortKey="Raveh, E" uniqKey="Raveh E">E. Raveh</name></author><author><name sortKey="Abu Lail, R" uniqKey="Abu Lail R">R. Abu-lail</name></author><author><name sortKey="Mezan, S" uniqKey="Mezan S">S. Mezan</name></author><author><name sortKey="Gilon, M" uniqKey="Gilon M">M. Gilon</name></author><author><name sortKey="Gershtain, E" uniqKey="Gershtain E">E. Gershtain</name></author><author><name sortKey="Birman, T" uniqKey="Birman T">T. Birman</name></author><author><name sortKey="Gallula, J" uniqKey="Gallula J">J. Gallula</name></author><author><name sortKey="Schneider, T" uniqKey="Schneider T">T. Schneider</name></author><author><name sortKey="Barkali, M" uniqKey="Barkali M">M. Barkali</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lu, R" uniqKey="Lu R">R. Lu</name></author><author><name sortKey="Zhang, J" uniqKey="Zhang J">J. Zhang</name></author><author><name sortKey="Zhang, W" uniqKey="Zhang W">W. Zhang</name></author><author><name sortKey="Huang, Y" uniqKey="Huang Y">Y. Huang</name></author><author><name sortKey="Wang, N" uniqKey="Wang N">N. Wang</name></author><author><name sortKey="Zhang, Q" uniqKey="Zhang Q">Q. Zhang</name></author><author><name sortKey="Qu, S" uniqKey="Qu S">S. Qu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Barkan, D" uniqKey="Barkan D">D. Barkan</name></author><author><name sortKey="Kleinman, H" uniqKey="Kleinman H">H. Kleinman</name></author><author><name sortKey="Simmons, J" uniqKey="Simmons J">J. Simmons</name></author><author><name sortKey="Asmussen, H" uniqKey="Asmussen H">H. Asmussen</name></author><author><name sortKey="Kamaraju, A" uniqKey="Kamaraju A">A. Kamaraju</name></author><author><name sortKey="Hoenorhoff, M" uniqKey="Hoenorhoff M">M. Hoenorhoff</name></author><author><name sortKey="Liu, Z" uniqKey="Liu Z">Z. Liu</name></author><author><name sortKey="Costes, S" uniqKey="Costes S">S. Costes</name></author><author><name sortKey="Cho, E" uniqKey="Cho E">E. Cho</name></author><author><name sortKey="Lockett, S" uniqKey="Lockett S">S. Lockett</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ren, Y" uniqKey="Ren Y">Y. Ren</name></author><author><name sortKey="Jia, H H" uniqKey="Jia H">H.H. Jia</name></author><author><name sortKey="Xu, Y Q" uniqKey="Xu Y">Y.Q. Xu</name></author><author><name sortKey="Zhou, X" uniqKey="Zhou X">X. Zhou</name></author><author><name sortKey="Zhao, X H" uniqKey="Zhao X">X.H. Zhao</name></author><author><name sortKey="Wang, Y F" uniqKey="Wang Y">Y.F. Wang</name></author><author><name sortKey="Song, X" uniqKey="Song X">X. Song</name></author><author><name sortKey="Zhu, Z Y" uniqKey="Zhu Z">Z.Y. Zhu</name></author><author><name sortKey="Sun, T" uniqKey="Sun T">T. Sun</name></author><author><name sortKey="Dou, Y" uniqKey="Dou Y">Y. Dou</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Teoh Fitzgerald, M L" uniqKey="Teoh Fitzgerald M">M.L. Teoh-Fitzgerald</name></author><author><name sortKey="Fitzgerald, M P" uniqKey="Fitzgerald M">M.P. Fitzgerald</name></author><author><name sortKey="Zhong, W" uniqKey="Zhong W">W. Zhong</name></author><author><name sortKey="Askeland, R W" uniqKey="Askeland R">R.W. Askeland</name></author><author><name sortKey="Domann, F E" uniqKey="Domann F">F.E. Domann</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lelievre, S A" uniqKey="Lelievre S">S.A. Lelièvre</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, M" uniqKey="Li M">M. Li</name></author><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author><author><name sortKey="Zhuang, Y" uniqKey="Zhuang Y">Y. Zhuang</name></author><author><name sortKey="Flemington, E K" uniqKey="Flemington E">E.K. Flemington</name></author><author><name sortKey="Lin, Z" uniqKey="Lin Z">Z. Lin</name></author><author><name sortKey="Shan, B" uniqKey="Shan B">B. Shan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gupta, R" uniqKey="Gupta R">R. Gupta</name></author><author><name sortKey="Shah, N" uniqKey="Shah N">N. Shah</name></author><author><name sortKey="Wang, K" uniqKey="Wang K">K. Wang</name></author><author><name sortKey="Kim, J" uniqKey="Kim J">J. Kim</name></author><author><name sortKey="Horlings, H" uniqKey="Horlings H">H. Horlings</name></author><author><name sortKey="Wong, D" uniqKey="Wong D">D. Wong</name></author><author><name sortKey="Tsai, M" uniqKey="Tsai M">M. Tsai</name></author><author><name sortKey="Hung, T" uniqKey="Hung T">T. Hung</name></author><author><name sortKey="Argani, P" uniqKey="Argani P">P. Argani</name></author><author><name sortKey="Rinn, J" uniqKey="Rinn J">J. Rinn</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y. Wang</name></author><author><name sortKey="Zhang, G" uniqKey="Zhang G">G. Zhang</name></author><author><name sortKey="Han, J" uniqKey="Han J">J. Han</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, M" uniqKey="Liu M">M. Liu</name></author><author><name sortKey="Xing, L" uniqKey="Xing L">L. Xing</name></author><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jia, X" uniqKey="Jia X">X. Jia</name></author><author><name sortKey="Shi, L" uniqKey="Shi L">L. Shi</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Luo, L" uniqKey="Luo L">L. Luo</name></author><author><name sortKey="Ling, L" uniqKey="Ling L">L. Ling</name></author><author><name sortKey="Yin, J" uniqKey="Yin J">J. Yin</name></author><author><name sortKey="Song, Y" uniqKey="Song Y">Y. Song</name></author><author><name sortKey="Zhang, Z" uniqKey="Zhang Z">Z. Zhang</name></author><author><name sortKey="Qiu, N" uniqKey="Qiu N">N. Qiu</name></author><author><name sortKey="Liu, H" uniqKey="Liu H">H. Liu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, B" uniqKey="Zhang B">B. Zhang</name></author><author><name sortKey="Arun, G" uniqKey="Arun G">G. Arun</name></author><author><name sortKey="Mao, Y S" uniqKey="Mao Y">Y.S. Mao</name></author><author><name sortKey="Lazar, Z" uniqKey="Lazar Z">Z. Lazar</name></author><author><name sortKey="Hung, G" uniqKey="Hung G">G. Hung</name></author><author><name sortKey="Bhattacharjee, G" uniqKey="Bhattacharjee G">G. Bhattacharjee</name></author><author><name sortKey="Xiao, X" uniqKey="Xiao X">X. Xiao</name></author><author><name sortKey="Booth, C J" uniqKey="Booth C">C.J. Booth</name></author><author><name sortKey="Wu, J" uniqKey="Wu J">J. Wu</name></author><author><name sortKey="Zhang, C" uniqKey="Zhang C">C. Zhang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Miao, Y" uniqKey="Miao Y">Y. Miao</name></author><author><name sortKey="Fan, R" uniqKey="Fan R">R. Fan</name></author><author><name sortKey="Chen, L" uniqKey="Chen L">L. Chen</name></author><author><name sortKey="Qian, H" uniqKey="Qian H">H. Qian</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jadaliha, M" uniqKey="Jadaliha M">M. Jadaliha</name></author><author><name sortKey="Zong, X" uniqKey="Zong X">X. Zong</name></author><author><name sortKey="Malakar, P" uniqKey="Malakar P">P. Malakar</name></author><author><name sortKey="Ray, T" uniqKey="Ray T">T. Ray</name></author><author><name sortKey="Singh, D K" uniqKey="Singh D">D.K. Singh</name></author><author><name sortKey="Freier, S M" uniqKey="Freier S">S.M. Freier</name></author><author><name sortKey="Jensen, T" uniqKey="Jensen T">T. Jensen</name></author><author><name sortKey="Prasanth, S G" uniqKey="Prasanth S">S.G. Prasanth</name></author><author><name sortKey="Karni, R" uniqKey="Karni R">R. Karni</name></author><author><name sortKey="Ray, P S" uniqKey="Ray P">P.S. Ray</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jin, C" uniqKey="Jin C">C. Jin</name></author><author><name sortKey="Yan, B" uniqKey="Yan B">B. Yan</name></author><author><name sortKey="Lu, Q" uniqKey="Lu Q">Q. Lu</name></author><author><name sortKey="Lin, Y" uniqKey="Lin Y">Y. Lin</name></author><author><name sortKey="Ma, L" uniqKey="Ma L">L. Ma</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author><author><name sortKey="Chen, N" uniqKey="Chen N">N. Chen</name></author><author><name sortKey="Zhou, L" uniqKey="Zhou L">L. Zhou</name></author><author><name sortKey="Wang, C" uniqKey="Wang C">C. Wang</name></author><author><name sortKey="Wen, X" uniqKey="Wen X">X. Wen</name></author><author><name sortKey="Jia, L" uniqKey="Jia L">L. Jia</name></author><author><name sortKey="Cui, J" uniqKey="Cui J">J. Cui</name></author><author><name sortKey="Hoffman, A" uniqKey="Hoffman A">A. Hoffman</name></author><author><name sortKey="Hu, J" uniqKey="Hu J">J. Hu</name></author><author><name sortKey="Li, W" uniqKey="Li W">W. Li</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, Z" uniqKey="Li Z">Z. Li</name></author><author><name sortKey="Xu, L" uniqKey="Xu L">L. Xu</name></author><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author><author><name sortKey="Fu, S" uniqKey="Fu S">S. Fu</name></author><author><name sortKey="Tu, J" uniqKey="Tu J">J. Tu</name></author><author><name sortKey="Hu, Y" uniqKey="Hu Y">Y. Hu</name></author><author><name sortKey="Xiong, Q" uniqKey="Xiong Q">Q. Xiong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stone, J" uniqKey="Stone J">J. Stone</name></author><author><name sortKey="Kim, J" uniqKey="Kim J">J. Kim</name></author><author><name sortKey="Vukadin, L" uniqKey="Vukadin L">L. Vukadin</name></author><author><name sortKey="Richard, A" uniqKey="Richard A">A. Richard</name></author><author><name sortKey="Giannini, H" uniqKey="Giannini H">H. Giannini</name></author><author><name sortKey="Lim, S" uniqKey="Lim S">S. Lim</name></author><author><name sortKey="Tan, M" uniqKey="Tan M">M. Tan</name></author><author><name sortKey="Ahn, E" uniqKey="Ahn E">E. Ahn</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Arun, G" uniqKey="Arun G">G. Arun</name></author><author><name sortKey="Diermeier, S" uniqKey="Diermeier S">S. Diermeier</name></author><author><name sortKey="Akerman, M" uniqKey="Akerman M">M. Akerman</name></author><author><name sortKey="Chang, K" uniqKey="Chang K">K. Chang</name></author><author><name sortKey="Wilkinson, J" uniqKey="Wilkinson J">J. Wilkinson</name></author><author><name sortKey="Hearn, S" uniqKey="Hearn S">S. Hearn</name></author><author><name sortKey="Kim, Y" uniqKey="Kim Y">Y. Kim</name></author><author><name sortKey="Macleod, A" uniqKey="Macleod A">A. MacLeod</name></author><author><name sortKey="Krainer, A" uniqKey="Krainer A">A. Krainer</name></author><author><name sortKey="Norton, L" uniqKey="Norton L">L. Norton</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zuo, Y" uniqKey="Zuo Y">Y. Zuo</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y. Li</name></author><author><name sortKey="Zhou, Z" uniqKey="Zhou Z">Z. Zhou</name></author><author><name sortKey="Ma, M" uniqKey="Ma M">M. Ma</name></author><author><name sortKey="Fu, K" uniqKey="Fu K">K. Fu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schneider, C" uniqKey="Schneider C">C. Schneider</name></author><author><name sortKey="King, R M" uniqKey="King R">R.M. King</name></author><author><name sortKey="Philipson, L" uniqKey="Philipson L">L. Philipson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Arshi, A" uniqKey="Arshi A">A. Arshi</name></author><author><name sortKey="Sharifi, F S" uniqKey="Sharifi F">F.S. Sharifi</name></author><author><name sortKey="Khorramian Ghahfarokhi, M" uniqKey="Khorramian Ghahfarokhi M">M. Khorramian Ghahfarokhi</name></author><author><name sortKey="Faghih, Z" uniqKey="Faghih Z">Z. Faghih</name></author><author><name sortKey="Doosti, A" uniqKey="Doosti A">A. Doosti</name></author><author><name sortKey="Ostovari, S" uniqKey="Ostovari S">S. Ostovari</name></author><author><name sortKey="Mahmoudi Maymand, E" uniqKey="Mahmoudi Maymand E">E. Mahmoudi Maymand</name></author><author><name sortKey="Ghahramani Seno, M M" uniqKey="Ghahramani Seno M">M.M. Ghahramani Seno</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, Z" uniqKey="Zhang Z">Z. Zhang</name></author><author><name sortKey="Zhu, Z" uniqKey="Zhu Z">Z. Zhu</name></author><author><name sortKey="Watabe, K" uniqKey="Watabe K">K. Watabe</name></author><author><name sortKey="Zhang, X" uniqKey="Zhang X">X. Zhang</name></author><author><name sortKey="Bai, C" uniqKey="Bai C">C. Bai</name></author><author><name sortKey="Xu, M" uniqKey="Xu M">M. Xu</name></author><author><name sortKey="Wu, F" uniqKey="Wu F">F. Wu</name></author><author><name sortKey="Mo, Y Y" uniqKey="Mo Y">Y.Y. Mo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, S" uniqKey="Li S">S. Li</name></author><author><name sortKey="Zhou, J" uniqKey="Zhou J">J. Zhou</name></author><author><name sortKey="Wang, Z" uniqKey="Wang Z">Z. Wang</name></author><author><name sortKey="Wang, P" uniqKey="Wang P">P. Wang</name></author><author><name sortKey="Gao, X" uniqKey="Gao X">X. Gao</name></author><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y. Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, L" uniqKey="Liu L">L. Liu</name></author><author><name sortKey="Yue, H" uniqKey="Yue H">H. Yue</name></author><author><name sortKey="Liu, Q" uniqKey="Liu Q">Q. Liu</name></author><author><name sortKey="Yuan, J" uniqKey="Yuan J">J. Yuan</name></author><author><name sortKey="Li, J" uniqKey="Li J">J. Li</name></author><author><name sortKey="Wei, G" uniqKey="Wei G">G. Wei</name></author><author><name sortKey="Chen, X" uniqKey="Chen X">X. Chen</name></author><author><name sortKey="Lu, Y" uniqKey="Lu Y">Y. Lu</name></author><author><name sortKey="Guo, M" uniqKey="Guo M">M. Guo</name></author><author><name sortKey="Luo, J" uniqKey="Luo J">J. Luo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xu, Y" uniqKey="Xu Y">Y. Xu</name></author><author><name sortKey="Zhang, G" uniqKey="Zhang G">G. Zhang</name></author><author><name sortKey="Zou, C" uniqKey="Zou C">C. Zou</name></author><author><name sortKey="Zhang, H" uniqKey="Zhang H">H. Zhang</name></author><author><name sortKey="Gong, Z" uniqKey="Gong Z">Z. Gong</name></author><author><name sortKey="Wang, W" uniqKey="Wang W">W. Wang</name></author><author><name sortKey="Ma, G" uniqKey="Ma G">G. Ma</name></author><author><name sortKey="Jiang, P" uniqKey="Jiang P">P. Jiang</name></author><author><name sortKey="Zhang, W" uniqKey="Zhang W">W. Zhang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, G" uniqKey="Zhang G">G. Zhang</name></author><author><name sortKey="Li, S" uniqKey="Li S">S. Li</name></author><author><name sortKey="Lu, J" uniqKey="Lu J">J. Lu</name></author><author><name sortKey="Ge, Y" uniqKey="Ge Y">Y. Ge</name></author><author><name sortKey="Wang, Q" uniqKey="Wang Q">Q. Wang</name></author><author><name sortKey="Ma, G" uniqKey="Ma G">G. Ma</name></author><author><name sortKey="Zhao, Q" uniqKey="Zhao Q">Q. Zhao</name></author><author><name sortKey="Wu, D" uniqKey="Wu D">D. Wu</name></author><author><name sortKey="Gong, W" uniqKey="Gong W">W. Gong</name></author><author><name sortKey="Du, M" uniqKey="Du M">M. Du</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhu, D" uniqKey="Zhu D">D. Zhu</name></author><author><name sortKey="Zhang, X" uniqKey="Zhang X">X. Zhang</name></author><author><name sortKey="Lin, Y" uniqKey="Lin Y">Y. Lin</name></author><author><name sortKey="Liang, S" uniqKey="Liang S">S. Liang</name></author><author><name sortKey="Song, Z" uniqKey="Song Z">Z. Song</name></author><author><name sortKey="Dong, C" uniqKey="Dong C">C. Dong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liang, Z" uniqKey="Liang Z">Z. Liang</name></author><author><name sortKey="Zhu, B" uniqKey="Zhu B">B. Zhu</name></author><author><name sortKey="Meng, D" uniqKey="Meng D">D. Meng</name></author><author><name sortKey="Shen, X" uniqKey="Shen X">X. Shen</name></author><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author><author><name sortKey="Wang, Z" uniqKey="Wang Z">Z. Wang</name></author><author><name sortKey="Li, L" uniqKey="Li L">L. Li</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chang, L" uniqKey="Chang L">L. Chang</name></author><author><name sortKey="Xu, W" uniqKey="Xu W">W. Xu</name></author><author><name sortKey="Zhang, Y" uniqKey="Zhang Y">Y. Zhang</name></author><author><name sortKey="Gong, F" uniqKey="Gong F">F. Gong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liang, W C" uniqKey="Liang W">W.C. Liang</name></author><author><name sortKey="Ren, J L" uniqKey="Ren J">J.L. Ren</name></author><author><name sortKey="Wong, C W" uniqKey="Wong C">C.W. Wong</name></author><author><name sortKey="Chan, S O" uniqKey="Chan S">S.O. Chan</name></author><author><name sortKey="Waye, M M" uniqKey="Waye M">M.M. Waye</name></author><author><name sortKey="Fu, W M" uniqKey="Fu W">W.M. Fu</name></author><author><name sortKey="Zhang, J F" uniqKey="Zhang J">J.F. Zhang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Song, X" uniqKey="Song X">X. Song</name></author><author><name sortKey="Liu, Z" uniqKey="Liu Z">Z. Liu</name></author><author><name sortKey="Yu, Z" uniqKey="Yu Z">Z. Yu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ke, S" uniqKey="Ke S">S. Ke</name></author><author><name sortKey="Li, R C" uniqKey="Li R">R.C. Li</name></author><author><name sortKey="Meng, F K" uniqKey="Meng F">F.K. Meng</name></author><author><name sortKey="Fang, M H" uniqKey="Fang M">M.H. Fang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wu, W" uniqKey="Wu W">W. Wu</name></author><author><name sortKey="Chen, F" uniqKey="Chen F">F. Chen</name></author><author><name sortKey="Cui, X" uniqKey="Cui X">X. Cui</name></author><author><name sortKey="Yang, L" uniqKey="Yang L">L. Yang</name></author><author><name sortKey="Chen, J" uniqKey="Chen J">J. Chen</name></author><author><name sortKey="Zhao, J" uniqKey="Zhao J">J. Zhao</name></author><author><name sortKey="Huang, D" uniqKey="Huang D">D. Huang</name></author><author><name sortKey="Liu, J" uniqKey="Liu J">J. Liu</name></author><author><name sortKey="Yang, L" uniqKey="Yang L">L. Yang</name></author><author><name sortKey="Zeng, J" uniqKey="Zeng J">J. Zeng</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, B" uniqKey="Liu B">B. Liu</name></author><author><name sortKey="Sun, L" uniqKey="Sun L">L. Sun</name></author><author><name sortKey="Liu, Q" uniqKey="Liu Q">Q. Liu</name></author><author><name sortKey="Gong, C" uniqKey="Gong C">C. Gong</name></author><author><name sortKey="Yao, Y" uniqKey="Yao Y">Y. Yao</name></author><author><name sortKey="Lv, X" uniqKey="Lv X">X. Lv</name></author><author><name sortKey="Lin, L" uniqKey="Lin L">L. Lin</name></author><author><name sortKey="Yao, H" uniqKey="Yao H">H. Yao</name></author><author><name sortKey="Su, F" uniqKey="Su F">F. Su</name></author><author><name sortKey="Li, D" uniqKey="Li D">D. Li</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhou, C X" uniqKey="Zhou C">C.X. Zhou</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Yang, N" uniqKey="Yang N">N. Yang</name></author><author><name sortKey="Xue, S K" uniqKey="Xue S">S.K. Xue</name></author><author><name sortKey="Li, W C" uniqKey="Li W">W.C. Li</name></author><author><name sortKey="Xie, P P" uniqKey="Xie P">P.P. Xie</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhou, B" uniqKey="Zhou B">B. Zhou</name></author><author><name sortKey="Guo, H" uniqKey="Guo H">H. Guo</name></author><author><name sortKey="Tang, J" uniqKey="Tang J">J. Tang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Beltran Anaya, F O" uniqKey="Beltran Anaya F">F.O. Beltran-Anaya</name></author><author><name sortKey="Romero Cordoba, S" uniqKey="Romero Cordoba S">S. Romero-Cordoba</name></author><author><name sortKey="Rebollar Vega, R" uniqKey="Rebollar Vega R">R. Rebollar-Vega</name></author><author><name sortKey="Arrieta, O" uniqKey="Arrieta O">O. Arrieta</name></author><author><name sortKey="Bautista Pina, V" uniqKey="Bautista Pina V">V. Bautista-Pina</name></author><author><name sortKey="Dominguez Reyes, C" uniqKey="Dominguez Reyes C">C. Dominguez-Reyes</name></author><author><name sortKey="Villegas Carlos, F" uniqKey="Villegas Carlos F">F. Villegas-Carlos</name></author><author><name sortKey="Tenorio Torres, A" uniqKey="Tenorio Torres A">A. Tenorio-Torres</name></author><author><name sortKey="Alfaro Riuz, L" uniqKey="Alfaro Riuz L">L. Alfaro-Riuz</name></author><author><name sortKey="Jimenez Morales, S" uniqKey="Jimenez Morales S">S. Jimenez-Morales</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Curtis, C" uniqKey="Curtis C">C. Curtis</name></author><author><name sortKey="Shah, S" uniqKey="Shah S">S. Shah</name></author><author><name sortKey="Chin, S" uniqKey="Chin S">S. Chin</name></author><author><name sortKey="Turashvili, G" uniqKey="Turashvili G">G. Turashvili</name></author><author><name sortKey="Rueda, O" uniqKey="Rueda O">O. Rueda</name></author><author><name sortKey="Dunning, M" uniqKey="Dunning M">M. Dunning</name></author><author><name sortKey="Speed, D" uniqKey="Speed D">D. Speed</name></author><author><name sortKey="Lynch, A" uniqKey="Lynch A">A. Lynch</name></author><author><name sortKey="Samarajiwa, S" uniqKey="Samarajiwa S">S. Samarajiwa</name></author><author><name sortKey="Yuan, Y" uniqKey="Yuan Y">Y. Yuan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lanczky, A" uniqKey="Lanczky A">A. Lánczky</name></author><author><name sortKey="Nagy, A" uniqKey="Nagy A">Á. Nagy</name></author><author><name sortKey="Bottai, G" uniqKey="Bottai G">G. Bottai</name></author><author><name sortKey="Munkacsy, G" uniqKey="Munkacsy G">G. Munkácsy</name></author><author><name sortKey="Szab, A" uniqKey="Szab A">A. Szabó</name></author><author><name sortKey="Santarpia, L" uniqKey="Santarpia L">L. Santarpia</name></author><author><name sortKey="Gy Rffy, B" uniqKey="Gy Rffy B">B. Győrffy</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Anaya, J" uniqKey="Anaya J">J. Anaya</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kim, J" uniqKey="Kim J">J. Kim</name></author><author><name sortKey="Piao, H" uniqKey="Piao H">H. Piao</name></author><author><name sortKey="Kim, B" uniqKey="Kim B">B. Kim</name></author><author><name sortKey="Yao, F" uniqKey="Yao F">F. Yao</name></author><author><name sortKey="Han, Z" uniqKey="Han Z">Z. Han</name></author><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y. Wang</name></author><author><name sortKey="Xiao, Z" uniqKey="Xiao Z">Z. Xiao</name></author><author><name sortKey="Siverly, A" uniqKey="Siverly A">A. Siverly</name></author><author><name sortKey="Lawhon, S" uniqKey="Lawhon S">S. Lawhon</name></author><author><name sortKey="Ton, B" uniqKey="Ton B">B. Ton</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xu, S" uniqKey="Xu S">S. Xu</name></author><author><name sortKey="Sui, S" uniqKey="Sui S">S. Sui</name></author><author><name sortKey="Zhang, J" uniqKey="Zhang J">J. Zhang</name></author><author><name sortKey="Bai, N" uniqKey="Bai N">N. Bai</name></author><author><name sortKey="Shi, Q" uniqKey="Shi Q">Q. Shi</name></author><author><name sortKey="Zhang, G" uniqKey="Zhang G">G. Zhang</name></author><author><name sortKey="Gao, S" uniqKey="Gao S">S. Gao</name></author><author><name sortKey="You, Z" uniqKey="You Z">Z. You</name></author><author><name sortKey="Zhan, C" uniqKey="Zhan C">C. Zhan</name></author><author><name sortKey="Liu, F" uniqKey="Liu F">F. Liu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kwok, Z H" uniqKey="Kwok Z">Z.H. Kwok</name></author><author><name sortKey="Roche, V" uniqKey="Roche V">V. Roche</name></author><author><name sortKey="Chew, X H" uniqKey="Chew X">X.H. Chew</name></author><author><name sortKey="Fadieieva, A" uniqKey="Fadieieva A">A. Fadieieva</name></author><author><name sortKey="Tay, Y" uniqKey="Tay Y">Y. Tay</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chen, Z" uniqKey="Chen Z">Z. Chen</name></author><author><name sortKey="Liu, S" uniqKey="Liu S">S. Liu</name></author><author><name sortKey="Tian, L" uniqKey="Tian L">L. Tian</name></author><author><name sortKey="Wu, M" uniqKey="Wu M">M. Wu</name></author><author><name sortKey="Ai, F" uniqKey="Ai F">F. Ai</name></author><author><name sortKey="Tang, W" uniqKey="Tang W">W. Tang</name></author><author><name sortKey="Zhao, L" uniqKey="Zhao L">L. Zhao</name></author><author><name sortKey="Ding, J" uniqKey="Ding J">J. Ding</name></author><author><name sortKey="Zhang, L" uniqKey="Zhang L">L. Zhang</name></author><author><name sortKey="Tang, A" uniqKey="Tang A">A. Tang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, X X" uniqKey="Wang X">X.X. Wang</name></author><author><name sortKey="Guo, G C" uniqKey="Guo G">G.C. Guo</name></author><author><name sortKey="Qian, X K" uniqKey="Qian X">X.K. Qian</name></author><author><name sortKey="Dou, D W" uniqKey="Dou D">D.W. Dou</name></author><author><name sortKey="Zhang, Z" uniqKey="Zhang Z">Z. Zhang</name></author><author><name sortKey="Xu, X D" uniqKey="Xu X">X.D. Xu</name></author><author><name sortKey="Duan, X" uniqKey="Duan X">X. Duan</name></author><author><name sortKey="Pei, X H" uniqKey="Pei X">X.H. Pei</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wen, S Y" uniqKey="Wen S">S.Y. Wen</name></author><author><name sortKey="Lin, Y" uniqKey="Lin Y">Y. Lin</name></author><author><name sortKey="Yu, Y Q" uniqKey="Yu Y">Y.Q. Yu</name></author><author><name sortKey="Cao, S J" uniqKey="Cao S">S.J. Cao</name></author><author><name sortKey="Zhang, R" uniqKey="Zhang R">R. Zhang</name></author><author><name sortKey="Yang, X M" uniqKey="Yang X">X.M. Yang</name></author><author><name sortKey="Li, J" uniqKey="Li J">J. Li</name></author><author><name sortKey="Zhang, Y L" uniqKey="Zhang Y">Y.L. Zhang</name></author><author><name sortKey="Wang, Y H" uniqKey="Wang Y">Y.H. Wang</name></author><author><name sortKey="Ma, M Z" uniqKey="Ma M">M.Z. Ma</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Peng, T" uniqKey="Peng T">T. Peng</name></author><author><name sortKey="Zhou, L" uniqKey="Zhou L">L. Zhou</name></author><author><name sortKey="Zuo, L" uniqKey="Zuo L">L. Zuo</name></author><author><name sortKey="Luan, Y" uniqKey="Luan Y">Y. Luan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, J" uniqKey="Li J">J. Li</name></author><author><name sortKey="Bian, E B" uniqKey="Bian E">E.B. Bian</name></author><author><name sortKey="He, X J" uniqKey="He X">X.J. He</name></author><author><name sortKey="Ma, C C" uniqKey="Ma C">C.C. Ma</name></author><author><name sortKey="Zong, G" uniqKey="Zong G">G. Zong</name></author><author><name sortKey="Wang, H L" uniqKey="Wang H">H.L. Wang</name></author><author><name sortKey="Zhao, B" uniqKey="Zhao B">B. Zhao</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jiang, Y" uniqKey="Jiang Y">Y. Jiang</name></author><author><name sortKey="Lin, L" uniqKey="Lin L">L. Lin</name></author><author><name sortKey="Zhong, S" uniqKey="Zhong S">S. Zhong</name></author><author><name sortKey="Cai, Y" uniqKey="Cai Y">Y. Cai</name></author><author><name sortKey="Zhang, F" uniqKey="Zhang F">F. Zhang</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Miao, R" uniqKey="Miao R">R. Miao</name></author><author><name sortKey="Zhang, B" uniqKey="Zhang B">B. Zhang</name></author><author><name sortKey="Gao, S" uniqKey="Gao S">S. Gao</name></author><author><name sortKey="Hu, X" uniqKey="Hu X">X. Hu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Armanious, H" uniqKey="Armanious H">H. Armanious</name></author><author><name sortKey="Deschenes, J" uniqKey="Deschenes J">J. Deschenes</name></author><author><name sortKey="Gelebart, P" uniqKey="Gelebart P">P. Gelebart</name></author><author><name sortKey="Ghosh, S" uniqKey="Ghosh S">S. Ghosh</name></author><author><name sortKey="Mackey, J" uniqKey="Mackey J">J. Mackey</name></author><author><name sortKey="Lai, R" uniqKey="Lai R">R. Lai</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dembowy, J" uniqKey="Dembowy J">J. Dembowy</name></author><author><name sortKey="Adissu, H" uniqKey="Adissu H">H. Adissu</name></author><author><name sortKey="Liu, J" uniqKey="Liu J">J. Liu</name></author><author><name sortKey="Zacksenhaus, E" uniqKey="Zacksenhaus E">E. Zacksenhaus</name></author><author><name sortKey="Woodgett, J" uniqKey="Woodgett J">J. Woodgett</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Farago, M" uniqKey="Farago M">M. Farago</name></author><author><name sortKey="Dominguez, I" uniqKey="Dominguez I">I. Dominguez</name></author><author><name sortKey="Landesman Bollag, E" uniqKey="Landesman Bollag E">E. Landesman-Bollag</name></author><author><name sortKey="Xu, X" uniqKey="Xu X">X. Xu</name></author><author><name sortKey="Rosner, A" uniqKey="Rosner A">A. Rosner</name></author><author><name sortKey="Cardiff, R" uniqKey="Cardiff R">R. Cardiff</name></author><author><name sortKey="Seldin, D" uniqKey="Seldin D">D. Seldin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shakoori, A" uniqKey="Shakoori A">A. Shakoori</name></author><author><name sortKey="Mai, W" uniqKey="Mai W">W. Mai</name></author><author><name sortKey="Miyashita, K" uniqKey="Miyashita K">K. Miyashita</name></author><author><name sortKey="Yasumoto, K" uniqKey="Yasumoto K">K. Yasumoto</name></author><author><name sortKey="Takahashi, Y" uniqKey="Takahashi Y">Y. Takahashi</name></author><author><name sortKey="Ooi, A" uniqKey="Ooi A">A. Ooi</name></author><author><name sortKey="Kawakami, K" uniqKey="Kawakami K">K. Kawakami</name></author><author><name sortKey="Minamoto, T" uniqKey="Minamoto T">T. Minamoto</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bilim, V" uniqKey="Bilim V">V. Bilim</name></author><author><name sortKey="Ougolkov, A" uniqKey="Ougolkov A">A. Ougolkov</name></author><author><name sortKey="Yuuki, K" uniqKey="Yuuki K">K. Yuuki</name></author><author><name sortKey="Naito, S" uniqKey="Naito S">S. Naito</name></author><author><name sortKey="Kawazoe, H" uniqKey="Kawazoe H">H. Kawazoe</name></author><author><name sortKey="Muto, A" uniqKey="Muto A">A. Muto</name></author><author><name sortKey="Oya, M" uniqKey="Oya M">M. Oya</name></author><author><name sortKey="Billadeau, D" uniqKey="Billadeau D">D. Billadeau</name></author><author><name sortKey="Motoyama, T" uniqKey="Motoyama T">T. Motoyama</name></author><author><name sortKey="Tomita, Y" uniqKey="Tomita Y">Y. Tomita</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xu, R" uniqKey="Xu R">R. Xu</name></author><author><name sortKey="Zhu, X" uniqKey="Zhu X">X. Zhu</name></author><author><name sortKey="Chen, F" uniqKey="Chen F">F. Chen</name></author><author><name sortKey="Huang, C" uniqKey="Huang C">C. Huang</name></author><author><name sortKey="Ai, K" uniqKey="Ai K">K. Ai</name></author><author><name sortKey="Wu, H" uniqKey="Wu H">H. Wu</name></author><author><name sortKey="Zhang, L" uniqKey="Zhang L">L. Zhang</name></author><author><name sortKey="Zhao, X" uniqKey="Zhao X">X. Zhao</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tang, Y" uniqKey="Tang Y">Y. Tang</name></author><author><name sortKey="He, R" uniqKey="He R">R. He</name></author><author><name sortKey="An, J" uniqKey="An J">J. An</name></author><author><name sortKey="Deng, P" uniqKey="Deng P">P. Deng</name></author><author><name sortKey="Huang, L" uniqKey="Huang L">L. Huang</name></author><author><name sortKey="Yang, W" uniqKey="Yang W">W. Yang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zheng, R" uniqKey="Zheng R">R. Zheng</name></author><author><name sortKey="Lin, S" uniqKey="Lin S">S. Lin</name></author><author><name sortKey="Guan, L" uniqKey="Guan L">L. Guan</name></author><author><name sortKey="Yuan, H" uniqKey="Yuan H">H. Yuan</name></author><author><name sortKey="Liu, K" uniqKey="Liu K">K. Liu</name></author><author><name sortKey="Liu, C" uniqKey="Liu C">C. Liu</name></author><author><name sortKey="Ye, W" uniqKey="Ye W">W. Ye</name></author><author><name sortKey="Liao, Y" uniqKey="Liao Y">Y. Liao</name></author><author><name sortKey="Jia, J" uniqKey="Jia J">J. Jia</name></author><author><name sortKey="Zhang, R" uniqKey="Zhang R">R. Zhang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hashimoto, S" uniqKey="Hashimoto S">S. Hashimoto</name></author><author><name sortKey="Amaya, F" uniqKey="Amaya F">F. Amaya</name></author><author><name sortKey="Matsuyama, H" uniqKey="Matsuyama H">H. Matsuyama</name></author><author><name sortKey="Ueno, H" uniqKey="Ueno H">H. Ueno</name></author><author><name sortKey="Kikuchi, S" uniqKey="Kikuchi S">S. Kikuchi</name></author><author><name sortKey="Tanaka, M" uniqKey="Tanaka M">M. Tanaka</name></author><author><name sortKey="Watanabe, Y" uniqKey="Watanabe Y">Y. Watanabe</name></author><author><name sortKey="Ebina, M" uniqKey="Ebina M">M. Ebina</name></author><author><name sortKey="Ishizaka, A" uniqKey="Ishizaka A">A. Ishizaka</name></author><author><name sortKey="Tsukita, S" uniqKey="Tsukita S">S. Tsukita</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xing, F" uniqKey="Xing F">F. Xing</name></author><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author><author><name sortKey="Wu, S Y" uniqKey="Wu S">S.Y. Wu</name></author><author><name sortKey="Wu, K" uniqKey="Wu K">K. Wu</name></author><author><name sortKey="Sharma, S" uniqKey="Sharma S">S. Sharma</name></author><author><name sortKey="Mo, Y Y" uniqKey="Mo Y">Y.Y. Mo</name></author><author><name sortKey="Feng, J" uniqKey="Feng J">J. Feng</name></author><author><name sortKey="Sanders, S" uniqKey="Sanders S">S. Sanders</name></author><author><name sortKey="Jin, G" uniqKey="Jin G">G. Jin</name></author><author><name sortKey="Singh, R" uniqKey="Singh R">R. Singh</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Salter, M W" uniqKey="Salter M">M.W. Salter</name></author><author><name sortKey="Stevens, B" uniqKey="Stevens B">B. Stevens</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Reya, T" uniqKey="Reya T">T. Reya</name></author><author><name sortKey="Morrison, S J" uniqKey="Morrison S">S.J. Morrison</name></author><author><name sortKey="Clarke, M F" uniqKey="Clarke M">M.F. Clarke</name></author><author><name sortKey="Weissman, I L" uniqKey="Weissman I">I.L. Weissman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Adorno Cruz, V" uniqKey="Adorno Cruz V">V. Adorno-Cruz</name></author><author><name sortKey="Kibria, G" uniqKey="Kibria G">G. Kibria</name></author><author><name sortKey="Liu, X" uniqKey="Liu X">X. Liu</name></author><author><name sortKey="Doherty, M" uniqKey="Doherty M">M. Doherty</name></author><author><name sortKey="Junk, D J" uniqKey="Junk D">D.J. Junk</name></author><author><name sortKey="Guan, D" uniqKey="Guan D">D. Guan</name></author><author><name sortKey="Hubert, C" uniqKey="Hubert C">C. Hubert</name></author><author><name sortKey="Venere, M" uniqKey="Venere M">M. Venere</name></author><author><name sortKey="Mulkearns Hubert, E" uniqKey="Mulkearns Hubert E">E. Mulkearns-Hubert</name></author><author><name sortKey="Sinyuk, M" uniqKey="Sinyuk M">M. Sinyuk</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Baccelli, I" uniqKey="Baccelli I">I. Baccelli</name></author><author><name sortKey="Trumpp, A" uniqKey="Trumpp A">A. Trumpp</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Antoniou, A" uniqKey="Antoniou A">A. Antoniou</name></author><author><name sortKey="Hebrant, A" uniqKey="Hebrant A">A. Hebrant</name></author><author><name sortKey="Dom, G" uniqKey="Dom G">G. Dom</name></author><author><name sortKey="Dumont, J E" uniqKey="Dumont J">J.E. Dumont</name></author><author><name sortKey="Maenhaut, C" uniqKey="Maenhaut C">C. Maenhaut</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Castro Oropeza, R" uniqKey="Castro Oropeza R">R. Castro-Oropeza</name></author><author><name sortKey="Melendez Zajgla, J" uniqKey="Melendez Zajgla J">J. Melendez-Zajgla</name></author><author><name sortKey="Maldonado, V" uniqKey="Maldonado V">V. Maldonado</name></author><author><name sortKey="Vazquez Santillan, K" uniqKey="Vazquez Santillan K">K. Vazquez-Santillan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mani, S" uniqKey="Mani S">S. Mani</name></author><author><name sortKey="Guo, W" uniqKey="Guo W">W. Guo</name></author><author><name sortKey="Liao, M" uniqKey="Liao M">M. Liao</name></author><author><name sortKey="Eaton, E" uniqKey="Eaton E">E. Eaton</name></author><author><name sortKey="Ayyanan, A" uniqKey="Ayyanan A">A. Ayyanan</name></author><author><name sortKey="Zhou, A" uniqKey="Zhou A">A. Zhou</name></author><author><name sortKey="Brooks, M" uniqKey="Brooks M">M. Brooks</name></author><author><name sortKey="Reinhard, F" uniqKey="Reinhard F">F. Reinhard</name></author><author><name sortKey="Zhang, C" uniqKey="Zhang C">C. Zhang</name></author><author><name sortKey="Shipitsin, M" uniqKey="Shipitsin M">M. Shipitsin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hardin, H" uniqKey="Hardin H">H. Hardin</name></author><author><name sortKey="Zhang, R" uniqKey="Zhang R">R. Zhang</name></author><author><name sortKey="Helein, H" uniqKey="Helein H">H. Helein</name></author><author><name sortKey="Buehler, D" uniqKey="Buehler D">D. Buehler</name></author><author><name sortKey="Guo, Z" uniqKey="Guo Z">Z. Guo</name></author><author><name sortKey="Lloyd, R V" uniqKey="Lloyd R">R.V. Lloyd</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, H" uniqKey="Li H">H. Li</name></author><author><name sortKey="Zhu, L" uniqKey="Zhu L">L. Zhu</name></author><author><name sortKey="Xu, L" uniqKey="Xu L">L. Xu</name></author><author><name sortKey="Qin, K" uniqKey="Qin K">K. Qin</name></author><author><name sortKey="Liu, C" uniqKey="Liu C">C. Liu</name></author><author><name sortKey="Yu, Y" uniqKey="Yu Y">Y. Yu</name></author><author><name sortKey="Su, D" uniqKey="Su D">D. Su</name></author><author><name sortKey="Wu, K" uniqKey="Wu K">K. Wu</name></author><author><name sortKey="Sheng, Y" uniqKey="Sheng Y">Y. Sheng</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Keshavarz, M" uniqKey="Keshavarz M">M. Keshavarz</name></author><author><name sortKey="Asadi, M H" uniqKey="Asadi M">M.H. Asadi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhou, M" uniqKey="Zhou M">M. Zhou</name></author><author><name sortKey="Hou, Y" uniqKey="Hou Y">Y. Hou</name></author><author><name sortKey="Yang, G" uniqKey="Yang G">G. Yang</name></author><author><name sortKey="Zhang, H" uniqKey="Zhang H">H. Zhang</name></author><author><name sortKey="Tu, G" uniqKey="Tu G">G. Tu</name></author><author><name sortKey="Du, Y E" uniqKey="Du Y">Y.E. Du</name></author><author><name sortKey="Wen, S" uniqKey="Wen S">S. Wen</name></author><author><name sortKey="Xu, L" uniqKey="Xu L">L. Xu</name></author><author><name sortKey="Tang, X" uniqKey="Tang X">X. Tang</name></author><author><name sortKey="Tang, S" uniqKey="Tang S">S. Tang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Deng, J" uniqKey="Deng J">J. Deng</name></author><author><name sortKey="Yang, M" uniqKey="Yang M">M. Yang</name></author><author><name sortKey="Jiang, R" uniqKey="Jiang R">R. Jiang</name></author><author><name sortKey="An, N" uniqKey="An N">N. An</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Liu, B" uniqKey="Liu B">B. Liu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, Z" uniqKey="Zhang Z">Z. Zhang</name></author><author><name sortKey="Sun, L" uniqKey="Sun L">L. Sun</name></author><author><name sortKey="Zhang, Y" uniqKey="Zhang Y">Y. Zhang</name></author><author><name sortKey="Lu, G" uniqKey="Lu G">G. Lu</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y. Li</name></author><author><name sortKey="Wei, Z" uniqKey="Wei Z">Z. Wei</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lu, G" uniqKey="Lu G">G. Lu</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y. Li</name></author><author><name sortKey="Ma, Y" uniqKey="Ma Y">Y. Ma</name></author><author><name sortKey="Lu, J" uniqKey="Lu J">J. Lu</name></author><author><name sortKey="Chen, Y" uniqKey="Chen Y">Y. Chen</name></author><author><name sortKey="Jiang, Q" uniqKey="Jiang Q">Q. Jiang</name></author><author><name sortKey="Qin, Q" uniqKey="Qin Q">Q. Qin</name></author><author><name sortKey="Zhao, L" uniqKey="Zhao L">L. Zhao</name></author><author><name sortKey="Huang, Q" uniqKey="Huang Q">Q. Huang</name></author><author><name sortKey="Luo, Z" uniqKey="Luo Z">Z. Luo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Huang, H" uniqKey="Huang H">H. Huang</name></author><author><name sortKey="Weng, H" uniqKey="Weng H">H. Weng</name></author><author><name sortKey="Sun, W" uniqKey="Sun W">W. Sun</name></author><author><name sortKey="Qin, X" uniqKey="Qin X">X. Qin</name></author><author><name sortKey="Shi, H" uniqKey="Shi H">H. Shi</name></author><author><name sortKey="Wu, H" uniqKey="Wu H">H. Wu</name></author><author><name sortKey="Zhao, B S" uniqKey="Zhao B">B.S. Zhao</name></author><author><name sortKey="Mesquita, A" uniqKey="Mesquita A">A. Mesquita</name></author><author><name sortKey="Liu, C" uniqKey="Liu C">C. Liu</name></author><author><name sortKey="Yuan, C L" uniqKey="Yuan C">C.L. Yuan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ma, F" uniqKey="Ma F">F. Ma</name></author><author><name sortKey="Liu, X" uniqKey="Liu X">X. Liu</name></author><author><name sortKey="Zhou, S" uniqKey="Zhou S">S. Zhou</name></author><author><name sortKey="Li, W" uniqKey="Li W">W. Li</name></author><author><name sortKey="Liu, C" uniqKey="Liu C">C. Liu</name></author><author><name sortKey="Chadwick, M" uniqKey="Chadwick M">M. Chadwick</name></author><author><name sortKey="Qian, C" uniqKey="Qian C">C. Qian</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, S" uniqKey="Zhang S">S. Zhang</name></author><author><name sortKey="Hu, X" uniqKey="Hu X">X. Hu</name></author><author><name sortKey="Zhang, W" uniqKey="Zhang W">W. Zhang</name></author><author><name sortKey="Tam, K" uniqKey="Tam K">K. Tam</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Peng, F" uniqKey="Peng F">F. Peng</name></author><author><name sortKey="Wang, J H" uniqKey="Wang J">J.H. Wang</name></author><author><name sortKey="Fan, W J" uniqKey="Fan W">W.J. Fan</name></author><author><name sortKey="Meng, Y T" uniqKey="Meng Y">Y.T. Meng</name></author><author><name sortKey="Li, M M" uniqKey="Li M">M.M. Li</name></author><author><name sortKey="Li, T T" uniqKey="Li T">T.T. Li</name></author><author><name sortKey="Cui, B" uniqKey="Cui B">B. Cui</name></author><author><name sortKey="Wang, H F" uniqKey="Wang H">H.F. Wang</name></author><author><name sortKey="Zhao, Y" uniqKey="Zhao Y">Y. Zhao</name></author><author><name sortKey="An, F" uniqKey="An F">F. An</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dupuy, F" uniqKey="Dupuy F">F. Dupuy</name></author><author><name sortKey="Tabaries, S" uniqKey="Tabaries S">S. Tabariès</name></author><author><name sortKey="Andrzejewski, S" uniqKey="Andrzejewski S">S. Andrzejewski</name></author><author><name sortKey="Dong, Z" uniqKey="Dong Z">Z. Dong</name></author><author><name sortKey="Blagih, J" uniqKey="Blagih J">J. Blagih</name></author><author><name sortKey="Annis, M" uniqKey="Annis M">M. Annis</name></author><author><name sortKey="Omeroglu, A" uniqKey="Omeroglu A">A. Omeroglu</name></author><author><name sortKey="Gao, D" uniqKey="Gao D">D. Gao</name></author><author><name sortKey="Leung, S" uniqKey="Leung S">S. Leung</name></author><author><name sortKey="Amir, E" uniqKey="Amir E">E. Amir</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Velpula, K" uniqKey="Velpula K">K. Velpula</name></author><author><name sortKey="Bhasin, A" uniqKey="Bhasin A">A. Bhasin</name></author><author><name sortKey="Asuthkar, S" uniqKey="Asuthkar S">S. Asuthkar</name></author><author><name sortKey="Tsung, A" uniqKey="Tsung A">A. Tsung</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, C" uniqKey="Li C">C. Li</name></author><author><name sortKey="Shan, S" uniqKey="Shan S">S. Shan</name></author><author><name sortKey="Huang, Q" uniqKey="Huang Q">Q. Huang</name></author><author><name sortKey="Braun, R" uniqKey="Braun R">R. Braun</name></author><author><name sortKey="Lanzen, J" uniqKey="Lanzen J">J. Lanzen</name></author><author><name sortKey="Hu, K" uniqKey="Hu K">K. Hu</name></author><author><name sortKey="Lin, P" uniqKey="Lin P">P. Lin</name></author><author><name sortKey="Dewhirst, M" uniqKey="Dewhirst M">M. Dewhirst</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Johnson, K E" uniqKey="Johnson K">K.E. Johnson</name></author><author><name sortKey="Wilgus, T A" uniqKey="Wilgus T">T.A. Wilgus</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Huang, X J" uniqKey="Huang X">X.J. Huang</name></author><author><name sortKey="Xia, Y" uniqKey="Xia Y">Y. Xia</name></author><author><name sortKey="He, G F" uniqKey="He G">G.F. He</name></author><author><name sortKey="Zheng, L L" uniqKey="Zheng L">L.L. Zheng</name></author><author><name sortKey="Cai, Y P" uniqKey="Cai Y">Y.P. Cai</name></author><author><name sortKey="Yin, Y" uniqKey="Yin Y">Y. Yin</name></author><author><name sortKey="Wu, Q" uniqKey="Wu Q">Q. Wu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Al Rugeebah, A" uniqKey="Al Rugeebah A">A. Al-Rugeebah</name></author><author><name sortKey="Alanazi, M" uniqKey="Alanazi M">M. Alanazi</name></author><author><name sortKey="Parine, N R" uniqKey="Parine N">N.R. Parine</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, C Y" uniqKey="Zhang C">C.Y. Zhang</name></author><author><name sortKey="Yu, M S" uniqKey="Yu M">M.S. Yu</name></author><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author><author><name sortKey="Zhang, Z" uniqKey="Zhang Z">Z. Zhang</name></author><author><name sortKey="Han, C R" uniqKey="Han C">C.R. Han</name></author><author><name sortKey="Yan, B" uniqKey="Yan B">B. Yan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Senkus, E" uniqKey="Senkus E">E. Senkus</name></author><author><name sortKey="Kyriakides, S" uniqKey="Kyriakides S">S. Kyriakides</name></author><author><name sortKey="Ohno, S" uniqKey="Ohno S">S. Ohno</name></author><author><name sortKey="Penault Llorca, F" uniqKey="Penault Llorca F">F. Penault-Llorca</name></author><author><name sortKey="Poortmans, P" uniqKey="Poortmans P">P. Poortmans</name></author><author><name sortKey="Rutgers, E" uniqKey="Rutgers E">E. Rutgers</name></author><author><name sortKey="Zackrisson, S" uniqKey="Zackrisson S">S. Zackrisson</name></author><author><name sortKey="Cardoso, F" uniqKey="Cardoso F">F. Cardoso</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Slamon, D" uniqKey="Slamon D">D. Slamon</name></author><author><name sortKey="Neven, P" uniqKey="Neven P">P. Neven</name></author><author><name sortKey="Chia, S" uniqKey="Chia S">S. Chia</name></author><author><name sortKey="Fasching, P" uniqKey="Fasching P">P. Fasching</name></author><author><name sortKey="De Laurentiis, M" uniqKey="De Laurentiis M">M. De Laurentiis</name></author><author><name sortKey="Im, S" uniqKey="Im S">S. Im</name></author><author><name sortKey="Petrakova, K" uniqKey="Petrakova K">K. Petrakova</name></author><author><name sortKey="Bianchi, G" uniqKey="Bianchi G">G. Bianchi</name></author><author><name sortKey="Esteva, F" uniqKey="Esteva F">F. Esteva</name></author><author><name sortKey="Martin, M" uniqKey="Martin M">M. Martín</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Vogel, C" uniqKey="Vogel C">C. Vogel</name></author><author><name sortKey="Cobleigh, M" uniqKey="Cobleigh M">M. Cobleigh</name></author><author><name sortKey="Tripathy, D" uniqKey="Tripathy D">D. Tripathy</name></author><author><name sortKey="Gutheil, J" uniqKey="Gutheil J">J. Gutheil</name></author><author><name sortKey="Harris, L" uniqKey="Harris L">L. Harris</name></author><author><name sortKey="Fehrenbacher, L" uniqKey="Fehrenbacher L">L. Fehrenbacher</name></author><author><name sortKey="Slamon, D" uniqKey="Slamon D">D. Slamon</name></author><author><name sortKey="Murphy, M" uniqKey="Murphy M">M. Murphy</name></author><author><name sortKey="Novotny, W" uniqKey="Novotny W">W. Novotny</name></author><author><name sortKey="Burchmore, M" uniqKey="Burchmore M">M. Burchmore</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Collins, D" uniqKey="Collins D">D. Collins</name></author><author><name sortKey="Conlon, N" uniqKey="Conlon N">N. Conlon</name></author><author><name sortKey="Kannan, S" uniqKey="Kannan S">S. Kannan</name></author><author><name sortKey="Verma, C" uniqKey="Verma C">C. Verma</name></author><author><name sortKey="Eli, L" uniqKey="Eli L">L. Eli</name></author><author><name sortKey="Lalani, A" uniqKey="Lalani A">A. Lalani</name></author><author><name sortKey="Crown, J" uniqKey="Crown J">J. Crown</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kim, S" uniqKey="Kim S">S. Kim</name></author><author><name sortKey="Dent, R" uniqKey="Dent R">R. Dent</name></author><author><name sortKey="Im, S" uniqKey="Im S">S. Im</name></author><author><name sortKey="Espie, M" uniqKey="Espie M">M. Espié</name></author><author><name sortKey="Blau, S" uniqKey="Blau S">S. Blau</name></author><author><name sortKey="Tan, A" uniqKey="Tan A">A. Tan</name></author><author><name sortKey="Isakoff, S" uniqKey="Isakoff S">S. Isakoff</name></author><author><name sortKey="Oliveira, M" uniqKey="Oliveira M">M. Oliveira</name></author><author><name sortKey="Saura, C" uniqKey="Saura C">C. Saura</name></author><author><name sortKey="Wongchenko, M" uniqKey="Wongchenko M">M. Wongchenko</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pan, H" uniqKey="Pan H">H. Pan</name></author><author><name sortKey="Gray, R" uniqKey="Gray R">R. Gray</name></author><author><name sortKey="Braybrooke, J" uniqKey="Braybrooke J">J. Braybrooke</name></author><author><name sortKey="Davies, C" uniqKey="Davies C">C. Davies</name></author><author><name sortKey="Taylor, C" uniqKey="Taylor C">C. Taylor</name></author><author><name sortKey="Mcgale, P" uniqKey="Mcgale P">P. McGale</name></author><author><name sortKey="Peto, R" uniqKey="Peto R">R. Peto</name></author><author><name sortKey="Pritchard, K" uniqKey="Pritchard K">K. Pritchard</name></author><author><name sortKey="Bergh, J" uniqKey="Bergh J">J. Bergh</name></author><author><name sortKey="Dowsett, M" uniqKey="Dowsett M">M. Dowsett</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dong, H" uniqKey="Dong H">H. Dong</name></author><author><name sortKey="Hu, J" uniqKey="Hu J">J. Hu</name></author><author><name sortKey="Zou, K" uniqKey="Zou K">K. Zou</name></author><author><name sortKey="Ye, M" uniqKey="Ye M">M. Ye</name></author><author><name sortKey="Chen, Y" uniqKey="Chen Y">Y. Chen</name></author><author><name sortKey="Wu, C" uniqKey="Wu C">C. Wu</name></author><author><name sortKey="Chen, X" uniqKey="Chen X">X. Chen</name></author><author><name sortKey="Han, M" uniqKey="Han M">M. Han</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wu, Y" uniqKey="Wu Y">Y. Wu</name></author><author><name sortKey="Sarkissyan, M" uniqKey="Sarkissyan M">M. Sarkissyan</name></author><author><name sortKey="Vadgama, J V" uniqKey="Vadgama J">J.V. Vadgama</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author><author><name sortKey="Wang, S" uniqKey="Wang S">S. Wang</name></author><author><name sortKey="Li, Z" uniqKey="Li Z">Z. Li</name></author><author><name sortKey="Long, X" uniqKey="Long X">X. Long</name></author><author><name sortKey="Guo, Z" uniqKey="Guo Z">Z. Guo</name></author><author><name sortKey="Zhang, G" uniqKey="Zhang G">G. Zhang</name></author><author><name sortKey="Zu, J" uniqKey="Zu J">J. Zu</name></author><author><name sortKey="Chen, Y" uniqKey="Chen Y">Y. Chen</name></author><author><name sortKey="Wen, L" uniqKey="Wen L">L. Wen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author><author><name sortKey="Wang, S" uniqKey="Wang S">S. Wang</name></author><author><name sortKey="Li, Z" uniqKey="Li Z">Z. Li</name></author><author><name sortKey="Long, X" uniqKey="Long X">X. Long</name></author><author><name sortKey="Guo, Z" uniqKey="Guo Z">Z. Guo</name></author><author><name sortKey="Zhang, G" uniqKey="Zhang G">G. Zhang</name></author><author><name sortKey="Zu, J" uniqKey="Zu J">J. Zu</name></author><author><name sortKey="Chen, Y" uniqKey="Chen Y">Y. Chen</name></author><author><name sortKey="Wen, L" uniqKey="Wen L">L. Wen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hu, X" uniqKey="Hu X">X. Hu</name></author><author><name sortKey="Hou, P" uniqKey="Hou P">P. Hou</name></author><author><name sortKey="Li, T" uniqKey="Li T">T. Li</name></author><author><name sortKey="Quan, H" uniqKey="Quan H">H. Quan</name></author><author><name sortKey="Li, M" uniqKey="Li M">M. Li</name></author><author><name sortKey="Lin, T" uniqKey="Lin T">T. Lin</name></author><author><name sortKey="Liu, J" uniqKey="Liu J">J. Liu</name></author><author><name sortKey="Bai, J" uniqKey="Bai J">J. Bai</name></author><author><name sortKey="Zheng, J" uniqKey="Zheng J">J. Zheng</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sun, X" uniqKey="Sun X">X. Sun</name></author><author><name sortKey="Huang, T" uniqKey="Huang T">T. Huang</name></author><author><name sortKey="Zhang, C" uniqKey="Zhang C">C. Zhang</name></author><author><name sortKey="Zhang, S" uniqKey="Zhang S">S. Zhang</name></author><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y. Wang</name></author><author><name sortKey="Zhang, Q" uniqKey="Zhang Q">Q. Zhang</name></author><author><name sortKey="Liu, Z" uniqKey="Liu Z">Z. Liu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xiu, D" uniqKey="Xiu D">D. Xiu</name></author><author><name sortKey="Liu, G" uniqKey="Liu G">G. Liu</name></author><author><name sortKey="Yu, S" uniqKey="Yu S">S. Yu</name></author><author><name sortKey="Li, L" uniqKey="Li L">L. Li</name></author><author><name sortKey="Zhao, G" uniqKey="Zhao G">G. Zhao</name></author><author><name sortKey="Liu, L" uniqKey="Liu L">L. Liu</name></author><author><name sortKey="Li, X" uniqKey="Li X">X. Li</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liang, Y" uniqKey="Liang Y">Y. Liang</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y. Li</name></author><author><name sortKey="Song, X" uniqKey="Song X">X. Song</name></author><author><name sortKey="Zhang, N" uniqKey="Zhang N">N. Zhang</name></author><author><name sortKey="Sang, Y" uniqKey="Sang Y">Y. Sang</name></author><author><name sortKey="Zhang, H" uniqKey="Zhang H">H. Zhang</name></author><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author><author><name sortKey="Chen, B" uniqKey="Chen B">B. Chen</name></author><author><name sortKey="Zhao, W" uniqKey="Zhao W">W. Zhao</name></author><author><name sortKey="Wang, L" uniqKey="Wang L">L. Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Longley, D B" uniqKey="Longley D">D.B. Longley</name></author><author><name sortKey="Harkin, D P" uniqKey="Harkin D">D.P. Harkin</name></author><author><name sortKey="Johnston, P G" uniqKey="Johnston P">P.G. Johnston</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tacar, O" uniqKey="Tacar O">O. Tacar</name></author><author><name sortKey="Sriamornsak, P" uniqKey="Sriamornsak P">P. Sriamornsak</name></author><author><name sortKey="Dass, C R" uniqKey="Dass C">C.R. Dass</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Sun, M" uniqKey="Sun M">M. Sun</name></author><author><name sortKey="Wu, D" uniqKey="Wu D">D. Wu</name></author><author><name sortKey="Zhou, K" uniqKey="Zhou K">K. Zhou</name></author><author><name sortKey="Li, H" uniqKey="Li H">H. Li</name></author><author><name sortKey="Gong, X" uniqKey="Gong X">X. Gong</name></author><author><name sortKey="Wei, Q" uniqKey="Wei Q">Q. Wei</name></author><author><name sortKey="Du, M" uniqKey="Du M">M. Du</name></author><author><name sortKey="Lei, P" uniqKey="Lei P">P. Lei</name></author><author><name sortKey="Zha, J" uniqKey="Zha J">J. Zha</name></author><author><name sortKey="Zhu, H" uniqKey="Zhu H">H. Zhu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, K" uniqKey="Zhang K">K. Zhang</name></author><author><name sortKey="Luo, Z" uniqKey="Luo Z">Z. Luo</name></author><author><name sortKey="Zhang, Y" uniqKey="Zhang Y">Y. Zhang</name></author><author><name sortKey="Zhang, L" uniqKey="Zhang L">L. Zhang</name></author><author><name sortKey="Wu, L" uniqKey="Wu L">L. Wu</name></author><author><name sortKey="Liu, L" uniqKey="Liu L">L. Liu</name></author><author><name sortKey="Yang, J" uniqKey="Yang J">J. Yang</name></author><author><name sortKey="Song, X" uniqKey="Song X">X. Song</name></author><author><name sortKey="Liu, J" uniqKey="Liu J">J. Liu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Han, L" uniqKey="Han L">L. Han</name></author><author><name sortKey="Ma, P" uniqKey="Ma P">P. Ma</name></author><author><name sortKey="Liu, S M" uniqKey="Liu S">S.M. Liu</name></author><author><name sortKey="Zhou, X" uniqKey="Zhou X">X. Zhou</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bai, J" uniqKey="Bai J">J. Bai</name></author><author><name sortKey="Zhao, W Y" uniqKey="Zhao W">W.Y. Zhao</name></author><author><name sortKey="Li, W J" uniqKey="Li W">W.J. Li</name></author><author><name sortKey="Ying, Z W" uniqKey="Ying Z">Z.W. Ying</name></author><author><name sortKey="Jiang, D Q" uniqKey="Jiang D">D.Q. Jiang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, X M" uniqKey="Liu X">X.M. Liu</name></author><author><name sortKey="Yang, B" uniqKey="Yang B">B. Yang</name></author><author><name sortKey="Han, J" uniqKey="Han J">J. Han</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Meng, Y" uniqKey="Meng Y">Y. Meng</name></author><author><name sortKey="Liu, Y L" uniqKey="Liu Y">Y.L. Liu</name></author><author><name sortKey="Li, K" uniqKey="Li K">K. Li</name></author><author><name sortKey="Fu, T" uniqKey="Fu T">T. Fu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhao, W" uniqKey="Zhao W">W. Zhao</name></author><author><name sortKey="Wang, Z" uniqKey="Wang Z">Z. Wang</name></author><author><name sortKey="Fang, X" uniqKey="Fang X">X. Fang</name></author><author><name sortKey="Li, N" uniqKey="Li N">N. Li</name></author><author><name sortKey="Fang, J" uniqKey="Fang J">J. Fang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lv, M" uniqKey="Lv M">M. Lv</name></author><author><name sortKey="Xu, P" uniqKey="Xu P">P. Xu</name></author><author><name sortKey="Wu, Y" uniqKey="Wu Y">Y. Wu</name></author><author><name sortKey="Huang, L" uniqKey="Huang L">L. Huang</name></author><author><name sortKey="Li, W" uniqKey="Li W">W. Li</name></author><author><name sortKey="Lv, S" uniqKey="Lv S">S. Lv</name></author><author><name sortKey="Wu, X" uniqKey="Wu X">X. Wu</name></author><author><name sortKey="Zeng, X" uniqKey="Zeng X">X. Zeng</name></author><author><name sortKey="Shen, R" uniqKey="Shen R">R. Shen</name></author><author><name sortKey="Jia, X" uniqKey="Jia X">X. Jia</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, H" uniqKey="Zhang H">H. Zhang</name></author><author><name sortKey="Zhang, N" uniqKey="Zhang N">N. Zhang</name></author><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author><author><name sortKey="Su, P" uniqKey="Su P">P. Su</name></author><author><name sortKey="Liang, Y" uniqKey="Liang Y">Y. Liang</name></author><author><name sortKey="Li, Y" uniqKey="Li Y">Y. Li</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Chen, T" uniqKey="Chen T">T. Chen</name></author><author><name sortKey="Song, X" uniqKey="Song X">X. Song</name></author><author><name sortKey="Sang, Y" uniqKey="Sang Y">Y. Sang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, R H" uniqKey="Li R">R.H. Li</name></author><author><name sortKey="Chen, M" uniqKey="Chen M">M. Chen</name></author><author><name sortKey="Liu, J" uniqKey="Liu J">J. Liu</name></author><author><name sortKey="Shao, C C" uniqKey="Shao C">C.C. Shao</name></author><author><name sortKey="Guo, C P" uniqKey="Guo C">C.P. Guo</name></author><author><name sortKey="Wei, X L" uniqKey="Wei X">X.L. Wei</name></author><author><name sortKey="Li, Y C" uniqKey="Li Y">Y.C. Li</name></author><author><name sortKey="Huang, W H" uniqKey="Huang W">W.H. Huang</name></author><author><name sortKey="Zhang, G J" uniqKey="Zhang G">G.J. Zhang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fu, J" uniqKey="Fu J">J. Fu</name></author><author><name sortKey="Dong, G" uniqKey="Dong G">G. Dong</name></author><author><name sortKey="Shi, H" uniqKey="Shi H">H. Shi</name></author><author><name sortKey="Zhang, J" uniqKey="Zhang J">J. Zhang</name></author><author><name sortKey="Ning, Z" uniqKey="Ning Z">Z. Ning</name></author><author><name sortKey="Bao, X" uniqKey="Bao X">X. Bao</name></author><author><name sortKey="Liu, C" uniqKey="Liu C">C. Liu</name></author><author><name sortKey="Hu, J" uniqKey="Hu J">J. Hu</name></author><author><name sortKey="Liu, M" uniqKey="Liu M">M. Liu</name></author><author><name sortKey="Xiong, B" uniqKey="Xiong B">B. Xiong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shore, A N" uniqKey="Shore A">A.N. Shore</name></author><author><name sortKey="Rosen, J M" uniqKey="Rosen J">J.M. Rosen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chen, M" uniqKey="Chen M">M. Chen</name></author><author><name sortKey="Zhuang, C" uniqKey="Zhuang C">C. Zhuang</name></author><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author><author><name sortKey="Li, J" uniqKey="Li J">J. Li</name></author><author><name sortKey="Dai, F" uniqKey="Dai F">F. Dai</name></author><author><name sortKey="Xia, M" uniqKey="Xia M">M. Xia</name></author><author><name sortKey="Zhan, Y" uniqKey="Zhan Y">Y. Zhan</name></author><author><name sortKey="Lin, J" uniqKey="Lin J">J. Lin</name></author><author><name sortKey="Chen, Z" uniqKey="Chen Z">Z. Chen</name></author><author><name sortKey="He, A" uniqKey="He A">A. He</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Campbell, P" uniqKey="Campbell P">P. Campbell</name></author><author><name sortKey="Yachida, S" uniqKey="Yachida S">S. Yachida</name></author><author><name sortKey="Mudie, L" uniqKey="Mudie L">L. Mudie</name></author><author><name sortKey="Stephens, P" uniqKey="Stephens P">P. Stephens</name></author><author><name sortKey="Pleasance, E" uniqKey="Pleasance E">E. Pleasance</name></author><author><name sortKey="Stebbings, L" uniqKey="Stebbings L">L. Stebbings</name></author><author><name sortKey="Morsberger, L" uniqKey="Morsberger L">L. Morsberger</name></author><author><name sortKey="Latimer, C" uniqKey="Latimer C">C. Latimer</name></author><author><name sortKey="Mclaren, S" uniqKey="Mclaren S">S. McLaren</name></author><author><name sortKey="Lin, M" uniqKey="Lin M">M. Lin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wu, X" uniqKey="Wu X">X. Wu</name></author><author><name sortKey="Northcott, P" uniqKey="Northcott P">P. Northcott</name></author><author><name sortKey="Dubuc, A" uniqKey="Dubuc A">A. Dubuc</name></author><author><name sortKey="Dupuy, A" uniqKey="Dupuy A">A. Dupuy</name></author><author><name sortKey="Shih, D" uniqKey="Shih D">D. Shih</name></author><author><name sortKey="Witt, H" uniqKey="Witt H">H. Witt</name></author><author><name sortKey="Croul, S" uniqKey="Croul S">S. Croul</name></author><author><name sortKey="Bouffet, E" uniqKey="Bouffet E">E. Bouffet</name></author><author><name sortKey="Fults, D" uniqKey="Fults D">D. Fults</name></author><author><name sortKey="Eberhart, C" uniqKey="Eberhart C">C. Eberhart</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mizushima, N" uniqKey="Mizushima N">N. Mizushima</name></author><author><name sortKey="Yoshimori, T" uniqKey="Yoshimori T">T. Yoshimori</name></author><author><name sortKey="Ohsumi, Y" uniqKey="Ohsumi Y">Y. Ohsumi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kenific, C M" uniqKey="Kenific C">C.M. Kenific</name></author><author><name sortKey="Thorburn, A" uniqKey="Thorburn A">A. Thorburn</name></author><author><name sortKey="Debnath, J" uniqKey="Debnath J">J. Debnath</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Moraes, L A" uniqKey="Moraes L">L.A. Moraes</name></author><author><name sortKey="Kar, S" uniqKey="Kar S">S. Kar</name></author><author><name sortKey="Foo, S L" uniqKey="Foo S">S.L. Foo</name></author><author><name sortKey="Gu, T" uniqKey="Gu T">T. Gu</name></author><author><name sortKey="Toh, Y Q" uniqKey="Toh Y">Y.Q. Toh</name></author><author><name sortKey="Ampomah, P B" uniqKey="Ampomah P">P.B. Ampomah</name></author><author><name sortKey="Sachaphibulkij, K" uniqKey="Sachaphibulkij K">K. Sachaphibulkij</name></author><author><name sortKey="Yap, G" uniqKey="Yap G">G. Yap</name></author><author><name sortKey="Zharkova, O" uniqKey="Zharkova O">O. Zharkova</name></author><author><name sortKey="Lukman, H M" uniqKey="Lukman H">H.M. Lukman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gu, J" uniqKey="Gu J">J. Gu</name></author><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y. Wang</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Zhou, D" uniqKey="Zhou D">D. Zhou</name></author><author><name sortKey="Wang, X" uniqKey="Wang X">X. Wang</name></author><author><name sortKey="Zhou, M" uniqKey="Zhou M">M. Zhou</name></author><author><name sortKey="He, Z" uniqKey="He Z">Z. He</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ruiz, A" uniqKey="Ruiz A">A. Ruiz</name></author><author><name sortKey="Rockfield, S" uniqKey="Rockfield S">S. Rockfield</name></author><author><name sortKey="Taran, N" uniqKey="Taran N">N. Taran</name></author><author><name sortKey="Haller, E" uniqKey="Haller E">E. Haller</name></author><author><name sortKey="Engelman, R" uniqKey="Engelman R">R. Engelman</name></author><author><name sortKey="Flores, I" uniqKey="Flores I">I. Flores</name></author><author><name sortKey="Panina Bordignon, P" uniqKey="Panina Bordignon P">P. Panina-Bordignon</name></author><author><name sortKey="Nanjundan, M" uniqKey="Nanjundan M">M. Nanjundan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cao, Z" uniqKey="Cao Z">Z. Cao</name></author><author><name sortKey="Livas, T" uniqKey="Livas T">T. Livas</name></author><author><name sortKey="Kyprianou, N" uniqKey="Kyprianou N">N. Kyprianou</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lu, J" uniqKey="Lu J">J. Lu</name></author><author><name sortKey="Tan, M" uniqKey="Tan M">M. Tan</name></author><author><name sortKey="Cai, Q" uniqKey="Cai Q">Q. Cai</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, X" uniqKey="Liu X">X. Liu</name></author><author><name sortKey="Fu, Q" uniqKey="Fu Q">Q. Fu</name></author><author><name sortKey="Li, S" uniqKey="Li S">S. Li</name></author><author><name sortKey="Liang, N" uniqKey="Liang N">N. Liang</name></author><author><name sortKey="Li, F" uniqKey="Li F">F. Li</name></author><author><name sortKey="Li, C" uniqKey="Li C">C. Li</name></author><author><name sortKey="Sui, C" uniqKey="Sui C">C. Sui</name></author><author><name sortKey="Dionigi, G" uniqKey="Dionigi G">G. Dionigi</name></author><author><name sortKey="Sun, H" uniqKey="Sun H">H. Sun</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gordon, M" uniqKey="Gordon M">M. Gordon</name></author><author><name sortKey="Babbs, B" uniqKey="Babbs B">B. Babbs</name></author><author><name sortKey="Cochrane, D" uniqKey="Cochrane D">D. Cochrane</name></author><author><name sortKey="Bitler, B" uniqKey="Bitler B">B. Bitler</name></author><author><name sortKey="Richer, J" uniqKey="Richer J">J. Richer</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Seitz, A" uniqKey="Seitz A">A. Seitz</name></author><author><name sortKey="Christensen, L" uniqKey="Christensen L">L. Christensen</name></author><author><name sortKey="Christensen, E" uniqKey="Christensen E">E. Christensen</name></author><author><name sortKey="Faarkrog, K" uniqKey="Faarkrog K">K. Faarkrog</name></author><author><name sortKey="Ostenfeld, M" uniqKey="Ostenfeld M">M. Ostenfeld</name></author><author><name sortKey="Hedegaard, J" uniqKey="Hedegaard J">J. Hedegaard</name></author><author><name sortKey="Nordentoft, I" uniqKey="Nordentoft I">I. Nordentoft</name></author><author><name sortKey="Nielsen, M" uniqKey="Nielsen M">M. Nielsen</name></author><author><name sortKey="Palmfeldt, J" uniqKey="Palmfeldt J">J. Palmfeldt</name></author><author><name sortKey="Thomson, M" uniqKey="Thomson M">M. Thomson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dai, X" uniqKey="Dai X">X. Dai</name></author><author><name sortKey="Li, T" uniqKey="Li T">T. Li</name></author><author><name sortKey="Bai, Z" uniqKey="Bai Z">Z. Bai</name></author><author><name sortKey="Yang, Y" uniqKey="Yang Y">Y. Yang</name></author><author><name sortKey="Liu, X" uniqKey="Liu X">X. Liu</name></author><author><name sortKey="Zhan, J" uniqKey="Zhan J">J. Zhan</name></author><author><name sortKey="Shi, B" uniqKey="Shi B">B. Shi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Heimes, A S" uniqKey="Heimes A">A.S. Heimes</name></author><author><name sortKey="Madjar, K" uniqKey="Madjar K">K. Madjar</name></author><author><name sortKey="Edlund, K" uniqKey="Edlund K">K. Edlund</name></author><author><name sortKey="Battista, M J" uniqKey="Battista M">M.J. Battista</name></author><author><name sortKey="Almstedt, K" uniqKey="Almstedt K">K. Almstedt</name></author><author><name sortKey="Elger, T" uniqKey="Elger T">T. Elger</name></author><author><name sortKey="Krajnak, S" uniqKey="Krajnak S">S. Krajnak</name></author><author><name sortKey="Rahnenfuhrer, J" uniqKey="Rahnenfuhrer J">J. Rahnenführer</name></author><author><name sortKey="Brenner, W" uniqKey="Brenner W">W. Brenner</name></author><author><name sortKey="Hasenburg, A" uniqKey="Hasenburg A">A. Hasenburg</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mathias, C" uniqKey="Mathias C">C. Mathias</name></author><author><name sortKey="Zambalde, E" uniqKey="Zambalde E">E. Zambalde</name></author><author><name sortKey="Rask, P" uniqKey="Rask P">P. Rask</name></author><author><name sortKey="Gradia, D" uniqKey="Gradia D">D. Gradia</name></author><author><name sortKey="De Oliveira, J" uniqKey="De Oliveira J">J. de Oliveira</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bhan, A" uniqKey="Bhan A">A. Bhan</name></author><author><name sortKey="Hussain, I" uniqKey="Hussain I">I. Hussain</name></author><author><name sortKey="Ansari, K I" uniqKey="Ansari K">K.I. Ansari</name></author><author><name sortKey="Kasiri, S" uniqKey="Kasiri S">S. Kasiri</name></author><author><name sortKey="Bashyal, A" uniqKey="Bashyal A">A. Bashyal</name></author><author><name sortKey="Mandal, S S" uniqKey="Mandal S">S.S. Mandal</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, F" uniqKey="Yang F">F. Yang</name></author><author><name sortKey="Lyu, S" uniqKey="Lyu S">S. Lyu</name></author><author><name sortKey="Dong, S" uniqKey="Dong S">S. Dong</name></author><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author><author><name sortKey="Zhang, X" uniqKey="Zhang X">X. Zhang</name></author><author><name sortKey="Wang, O" uniqKey="Wang O">O. Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lehmann, B" uniqKey="Lehmann B">B. Lehmann</name></author><author><name sortKey="Bauer, J" uniqKey="Bauer J">J. Bauer</name></author><author><name sortKey="Chen, X" uniqKey="Chen X">X. Chen</name></author><author><name sortKey="Sanders, M" uniqKey="Sanders M">M. Sanders</name></author><author><name sortKey="Chakravarthy, A" uniqKey="Chakravarthy A">A. Chakravarthy</name></author><author><name sortKey="Shyr, Y" uniqKey="Shyr Y">Y. Shyr</name></author><author><name sortKey="Pietenpol, J" uniqKey="Pietenpol J">J. Pietenpol</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, E" uniqKey="Liu E">E. Liu</name></author><author><name sortKey="Liu, Z" uniqKey="Liu Z">Z. Liu</name></author><author><name sortKey="Zhou, Y" uniqKey="Zhou Y">Y. Zhou</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Martin, D" uniqKey="Martin D">D. Martin</name></author><author><name sortKey="Smith, C L" uniqKey="Smith C">C.L. Smith</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhao, Z" uniqKey="Zhao Z">Z. Zhao</name></author><author><name sortKey="Chen, C" uniqKey="Chen C">C. Chen</name></author><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author><author><name sortKey="Wu, C" uniqKey="Wu C">C. Wu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gupta, P B" uniqKey="Gupta P">P.B. Gupta</name></author><author><name sortKey="Pastushenko, I" uniqKey="Pastushenko I">I. Pastushenko</name></author><author><name sortKey="Skibinski, A" uniqKey="Skibinski A">A. Skibinski</name></author><author><name sortKey="Blanpain, C" uniqKey="Blanpain C">C. Blanpain</name></author><author><name sortKey="Kuperwasser, C" uniqKey="Kuperwasser C">C. Kuperwasser</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pastushenko, I" uniqKey="Pastushenko I">I. Pastushenko</name></author><author><name sortKey="Blanpain, C" uniqKey="Blanpain C">C. Blanpain</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Norouzi, S" uniqKey="Norouzi S">S. Norouzi</name></author><author><name sortKey="Gorgi Valokala, M" uniqKey="Gorgi Valokala M">M. Gorgi Valokala</name></author><author><name sortKey="Mosaffa, F" uniqKey="Mosaffa F">F. Mosaffa</name></author><author><name sortKey="Zirak, M" uniqKey="Zirak M">M. Zirak</name></author><author><name sortKey="Zamani, P" uniqKey="Zamani P">P. Zamani</name></author><author><name sortKey="Behravan, J" uniqKey="Behravan J">J. Behravan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lawson, D" uniqKey="Lawson D">D. Lawson</name></author><author><name sortKey="Kessenbrock, K" uniqKey="Kessenbrock K">K. Kessenbrock</name></author><author><name sortKey="Davis, R" uniqKey="Davis R">R. Davis</name></author><author><name sortKey="Pervolarakis, N" uniqKey="Pervolarakis N">N. Pervolarakis</name></author><author><name sortKey="Werb, Z" uniqKey="Werb Z">Z. Werb</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, Q" uniqKey="Wang Q">Q. Wang</name></author><author><name sortKey="Fan, H" uniqKey="Fan H">H. Fan</name></author><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y. Liu</name></author><author><name sortKey="Yin, Z" uniqKey="Yin Z">Z. Yin</name></author><author><name sortKey="Cai, H" uniqKey="Cai H">H. Cai</name></author><author><name sortKey="Liu, J" uniqKey="Liu J">J. Liu</name></author><author><name sortKey="Wang, Z" uniqKey="Wang Z">Z. Wang</name></author><author><name sortKey="Shao, M" uniqKey="Shao M">M. Shao</name></author><author><name sortKey="Sun, X" uniqKey="Sun X">X. Sun</name></author><author><name sortKey="Diao, J" uniqKey="Diao J">J. Diao</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hu, X" uniqKey="Hu X">X. Hu</name></author><author><name sortKey="Ding, D" uniqKey="Ding D">D. Ding</name></author><author><name sortKey="Zhang, J" uniqKey="Zhang J">J. Zhang</name></author><author><name sortKey="Cui, J" uniqKey="Cui J">J. Cui</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, Y" uniqKey="Zhang Y">Y. Zhang</name></author><author><name sortKey="He, Q" uniqKey="He Q">Q. He</name></author><author><name sortKey="Hu, Z" uniqKey="Hu Z">Z. Hu</name></author><author><name sortKey="Feng, Y" uniqKey="Feng Y">Y. Feng</name></author><author><name sortKey="Fan, L" uniqKey="Fan L">L. Fan</name></author><author><name sortKey="Tang, Z" uniqKey="Tang Z">Z. Tang</name></author><author><name sortKey="Yuan, J" uniqKey="Yuan J">J. Yuan</name></author><author><name sortKey="Shan, W" uniqKey="Shan W">W. Shan</name></author><author><name sortKey="Li, C" uniqKey="Li C">C. Li</name></author><author><name sortKey="Hu, X" uniqKey="Hu X">X. Hu</name></author></analytic></biblStruct></listBibl></div1></back></TEI><pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Cancers (Basel)</journal-id><journal-id journal-id-type="iso-abbrev">Cancers (Basel)</journal-id><journal-id journal-id-type="publisher-id">cancers</journal-id><journal-title-group><journal-title>Cancers</journal-title></journal-title-group><issn pub-type="epub">2072-6694</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31744046</article-id><article-id pub-id-type="pmc">6896003</article-id><article-id pub-id-type="doi">10.3390/cancers11111802</article-id><article-id pub-id-type="publisher-id">cancers-11-01802</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Long Non-Coding RNA: Dual Effects on Breast Cancer Metastasis and Clinical Applications</article-title></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0003-0731-3336</contrib-id><name><surname>Huang</surname><given-names>Qi-Yuan</given-names></name><xref ref-type="aff" rid="af1-cancers-11-01802">1</xref><xref ref-type="aff" rid="af2-cancers-11-01802">2</xref><xref ref-type="author-notes" rid="fn1-cancers-11-01802">†</xref></contrib><contrib contrib-type="author"><name><surname>Liu</surname><given-names>Guo-Feng</given-names></name><xref ref-type="aff" rid="af3-cancers-11-01802">3</xref><xref ref-type="author-notes" rid="fn1-cancers-11-01802">†</xref></contrib><contrib contrib-type="author"><name><surname>Qian</surname><given-names>Xian-Ling</given-names></name><xref ref-type="aff" rid="af1-cancers-11-01802">1</xref><xref ref-type="aff" rid="af3-cancers-11-01802">3</xref><xref ref-type="author-notes" rid="fn1-cancers-11-01802">†</xref></contrib><contrib contrib-type="author"><name><surname>Tang</surname><given-names>Li-Bo</given-names></name><xref ref-type="aff" rid="af1-cancers-11-01802">1</xref><xref ref-type="aff" rid="af2-cancers-11-01802">2</xref></contrib><contrib contrib-type="author"><name><surname>Huang</surname><given-names>Qing-Yun</given-names></name><xref ref-type="aff" rid="af1-cancers-11-01802">1</xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0003-3769-2496</contrib-id><name><surname>Xiong</surname><given-names>Li-Xia</given-names></name><xref ref-type="aff" rid="af1-cancers-11-01802">1</xref><xref ref-type="aff" rid="af4-cancers-11-01802">4</xref><xref rid="c1-cancers-11-01802" ref-type="corresp">*</xref></contrib></contrib-group><aff id="af1-cancers-11-01802"><label>1</label>Department of Pathophysiology, Basic Medical College, Nanchang University, Nanchang 330006, China;<email>6301616056@email.ncu.edu.cn</email> (Q.-Y.H.);<email>6302615051@email.ncu.edu.cn</email> (X.-L.Q.);<email>lb525912836@163.com</email> (L.-B.T.);<email>401442718029@email.ncu.edu.cn</email> (Q.-Y.H.)</aff><aff id="af2-cancers-11-01802"><label>2</label>Second Clinical Medical College, Nanchang University, Nanchang 330006, China</aff><aff id="af3-cancers-11-01802"><label>3</label>First Clinical Medical College, Nanchang University, Nanchang 330006, China;<email>6302615053@email.ncu.edu.cn</email></aff><aff id="af4-cancers-11-01802"><label>4</label>Jiangxi Province Key Laboratory of Tumor Pathogenesis and Molecular Pathology, Nanchang 330006, China</aff><author-notes><corresp id="c1-cancers-11-01802"><label>*</label>Correspondence: <email>xionglixia@ncu.edu.cn</email>; Tel.: +86-791-8636-0556</corresp><fn id="fn1-cancers-11-01802"><label>†</label><p>These authors contributed equally to this work.</p></fn></author-notes><pub-date pub-type="epub"><day>16</day><month>11</month><year>2019</year></pub-date><pub-date pub-type="collection"><month>11</month><year>2019</year></pub-date><volume>11</volume><issue>11</issue><elocation-id>1802</elocation-id><history><date date-type="received"><day>19</day><month>9</month><year>2019</year></date><date date-type="accepted"><day>12</day><month>11</month><year>2019</year></date></history><permissions><copyright-statement>© 2019 by the authors.</copyright-statement><copyright-year>2019</copyright-year><license license-type="open-access"><license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>).</license-p></license></permissions><abstract><p>As a highly heterogeneous malignancy, breast cancer (BC) has become the most significant threat to female health. Distant metastasis and therapy resistance of BC are responsible for most of the cases of mortality and recurrence. Distant metastasis relies on an array of processes, such as cell proliferation, epithelial-to-mesenchymal transition (EMT), mesenchymal-to-epithelial transition (MET), and angiogenesis. Long non-coding RNA (lncRNA) refers to a class of non-coding RNA with a length of over 200 nucleotides. Currently, a rising number of studies have managed to investigate the association between BC and lncRNA. In this study, we summarized how lncRNA has dual effects in BC metastasis by regulating invasion, migration, and distant metastasis of BC cells. We also emphasize that lncRNA has crucial regulatory effects in the stemness and angiogenesis of BC. Clinically, some lncRNAs can regulate chemotherapy sensitivity in BC patients and may function as novel biomarkers to diagnose or predict prognosis for BC patients. The exact impact on clinical relevance deserves further study. This review can be an approach to understanding the dual effects of lncRNAs in BC, thereby linking lncRNAs to quasi-personalized treatment in the future.</p></abstract><kwd-group><kwd>lncRNA</kwd><kwd>breast cancer</kwd><kwd>metastasis</kwd><kwd>cancer stem cell</kwd><kwd>angiogenesis</kwd><kwd>chemotherapy resistance</kwd><kwd>prognosis</kwd></kwd-group></article-meta></front><body><sec sec-type="intro" id="sec1-cancers-11-01802"><title>1. Introduction</title><p>Nowadays, breast cancer (BC) is one of the most common cancers on a global scale, and it is the main cause of cancer death in women. In 2018, the number of newly diagnosed female BC cases worldwide reached 2.1 million, accounting for nearly a quarter of female cancer cases [<xref rid="B1-cancers-11-01802" ref-type="bibr">1</xref>]. Metastasis is responsible for most cases of cancer mortality and relies on an array of processes, including the bilateral transition between epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET), promotion of cancer cell invasion, migration, stemness and metastasis, inhibition of cancer cell proliferation, anoikis, and post metastatic angiogenesis. Therefore, molecular mechanisms that affect any of these processes may be involved in regulating tumor metastasis.</p><p>Ever since the definition of four subtypes of BC (luminal A, luminal B, human epidermal growth factor receptor 2 positive (HER-2+), and basal-like), the clinical treatment for BC patients has become more specific and individualized. An increasing amount of mechanism research has made it possible to individualize treatment and achieve a better prognosis for patients. For example, in HER-2 overexpression patients, the successful application of anti-HER-2 drugs commendably demonstrates the advantages of the latest achievements in molecular science of basic medicine [<xref rid="B2-cancers-11-01802" ref-type="bibr">2</xref>]. Triple negative breast cancer (TNBC) is defined by the negative expression of estrogen receptors (ER), progesterone receptors (PR), and the lack of expression of HER-2 [<xref rid="B3-cancers-11-01802" ref-type="bibr">3</xref>]. Clinically, TNBC has high invasiveness and the metastasis rate is also abnormally high [<xref rid="B4-cancers-11-01802" ref-type="bibr">4</xref>]. A lack of receptor expression leads to a low chemotherapy response rate and poor efficiency of targeted therapy. Until now, there has been no clear and effective molecular targeted therapy for TNBC [<xref rid="B5-cancers-11-01802" ref-type="bibr">5</xref>]. Previous studies have demonstrated the crosstalk between tumor metastasis and therapy resistance in various cancers, including BC; among them, EMT regulation has a crucial role [<xref rid="B6-cancers-11-01802" ref-type="bibr">6</xref>]. Additionally, EMT programming in cancer cells enables the remodeling of the extracellular matrix to break the dormancy of relapse-initiating cancer stem cells (CSCs) [<xref rid="B7-cancers-11-01802" ref-type="bibr">7</xref>].</p><p>According to the encyclopedia of DNA elements (ENCODE) project, more than 80% of the human genome is transcribed into biochemically functional non-coding RNAs (ncRNAs) [<xref rid="B8-cancers-11-01802" ref-type="bibr">8</xref>]. Transfer RNAs (tRNAs), ribosomal RNAs (rRNAs), microRNAs (miRNAs), small nuclear RNAs (snRNAs), and long non-coding RNAs (lncRNAs) are all types of ncRNAs [<xref rid="B9-cancers-11-01802" ref-type="bibr">9</xref>]. LncRNAs are a class of ncRNA with a length over 200 nucleotides and can be divided into five categories according to the position of their DNA fragments in the genome, including bidirectional, antisense, intergenic, intronic, and sense lncRNAs [<xref rid="B10-cancers-11-01802" ref-type="bibr">10</xref>].</p><p>As part of the ENCODE consortium, GENCODE (version 32) annotated 17,910 lncRNA genes and 48,351 lncRNA transcripts [<xref rid="B11-cancers-11-01802" ref-type="bibr">11</xref>]. Among them, previous studies have indicated as many as 60,000 lncRNAs in humans and other mammals [<xref rid="B12-cancers-11-01802" ref-type="bibr">12</xref>]. The discovery of numerous lncRNA transcripts has dramatically altered our understanding of cell biology, especially the biology of underexamined diseases such as cancer. Currently, many studies have investigated the association between lncRNAs and cardiovascular disease [<xref rid="B13-cancers-11-01802" ref-type="bibr">13</xref>,<xref rid="B14-cancers-11-01802" ref-type="bibr">14</xref>], neurological diseases [<xref rid="B15-cancers-11-01802" ref-type="bibr">15</xref>,<xref rid="B16-cancers-11-01802" ref-type="bibr">16</xref>], diabetes [<xref rid="B17-cancers-11-01802" ref-type="bibr">17</xref>], cancer [<xref rid="B18-cancers-11-01802" ref-type="bibr">18</xref>], and more. LncRNAs function through a variety of molecular mechanisms, such as acting as scaffolds for ribonucleoprotein (RNP) complexes, decoys for transcriptional factors or miRNAs, RNA interference, targeting of transcriptional factors or chromatin modifier proteins to specific genomic loci, and transcriptional regulation in cis or trans [<xref rid="B19-cancers-11-01802" ref-type="bibr">19</xref>]. Interestingly, a number of studies have proposed that lncRNAs could inactivate miRNAs through a “sponge” effect, namely by sequestering miRNAs from their target mRNAs as a competing endogenous RNA (ceRNA) [<xref rid="B20-cancers-11-01802" ref-type="bibr">20</xref>,<xref rid="B21-cancers-11-01802" ref-type="bibr">21</xref>]. This interaction also exists during cancer progression [<xref rid="B22-cancers-11-01802" ref-type="bibr">22</xref>,<xref rid="B23-cancers-11-01802" ref-type="bibr">23</xref>]. In addition to basic research, the clinical application of lncRNAs is also an emerging research field [<xref rid="B24-cancers-11-01802" ref-type="bibr">24</xref>]. LncRNAs are ideal diagnostic biomarkers and therapeutic targets. As of yet, due to the lack of basic clinical research, lncRNAs have not been applied in commercial diagnostic tests.</p><p>In this study, we reviewed the latest progress in this area and found that lncRNAs not only have a role in regulating the aggressiveness of BC cells but also have an effect on the distant metastasis and therapy resistance in BC patients. To our surprise, we found that lncRNAs also have a role in regulating the stemness of cancer stem cells and tumor angiogenesis, affecting cancer metastasis. In addition, by reviewing a number of studies, we discuss whether and how lncRNAs facilitate the diagnosis and prognosis prediction and improve the specificity for therapy of BC by acting as biomarkers. A considerable number of studies have uncovered the effect of lncRNAs on BC metastasis via various signaling pathways, which is also a focus of this review.</p></sec><sec id="sec2-cancers-11-01802"><title>2. LncRNAs That Enhance Aggressiveness of BC Cells</title><sec id="sec2dot1-cancers-11-01802"><title>2.1. LncRNAs That Promote Invasion and Migration of BC Cells</title><sec id="sec2dot1dot1-cancers-11-01802"><title>2.1.1. DANCR</title><p>Previous studies have identified lncRNA differentiation antagonizing non-protein-coding RNA (lncRNA DANCR) associated with hepatocellular carcinoma, colorectal cancer, and BC, especially in TNBC [<xref rid="B25-cancers-11-01802" ref-type="bibr">25</xref>,<xref rid="B26-cancers-11-01802" ref-type="bibr">26</xref>,<xref rid="B27-cancers-11-01802" ref-type="bibr">27</xref>]. Knockdown of DANCR inhibited BC cell invasion and migration. Mechanistically, DANCR downregulation impaired the expression of CD44 and ATP binding cassette subfamily G member 2 (ABCG2) through enhancement of the zeste homolog 2 (EZH2) [<xref rid="B27-cancers-11-01802" ref-type="bibr">27</xref>]. EZH2 is a part of the polycomb repressive complex 2 (PRC2) that facilitates target gene silencing through trimethylation of histone 3 lysine 27 (H3K27) residues [<xref rid="B28-cancers-11-01802" ref-type="bibr">28</xref>]. DANCR suppression could have a negative effect on EZH2 and PRC2-mediated H3K27-trimethylation at the epigenetic level [<xref rid="B29-cancers-11-01802" ref-type="bibr">29</xref>]. Another potential mechanism was identified by bioinformatics analysis, which confirmed the DANCR/miRNA-216a-5p axis in TNBC cells, and DANCR knockdown resulted in inhibited cell invasion and decreased expression of Nanog, SRY-box containing gene 2 (SOX2), and octamer-binding transcription factor-4 (OCT4) [<xref rid="B30-cancers-11-01802" ref-type="bibr">30</xref>].</p></sec><sec id="sec2dot1dot2-cancers-11-01802"><title>2.1.2. H19</title><p>LncRNA H19 has been identified to be functionally associated with many biological processes, such as cell proliferation, invasion, and apoptosis of tumors, including in BC [<xref rid="B31-cancers-11-01802" ref-type="bibr">31</xref>,<xref rid="B32-cancers-11-01802" ref-type="bibr">32</xref>]. DNA hypermethylation is involved in BC carcinogenesis and cell survival, and is initiated by abnormal expression of DNA methyltransferases (DNMTs), such as DNMT1, DNMT3a, and DNMT3b [<xref rid="B33-cancers-11-01802" ref-type="bibr">33</xref>,<xref rid="B34-cancers-11-01802" ref-type="bibr">34</xref>,<xref rid="B35-cancers-11-01802" ref-type="bibr">35</xref>]. Evidence has indicated that H19 is aberrantly upregulated in BC and promotes invasion of BC cells via the miR-152/DNMT1 axis, and such outcomes can be reversed by miR-152 overexpression and DNMT1 knockdown [<xref rid="B36-cancers-11-01802" ref-type="bibr">36</xref>]. H19 and insulin-like growth factor 2 (IGF2) usually jointly accelerate cancer development of mammary and pulmonary tumors [<xref rid="B37-cancers-11-01802" ref-type="bibr">37</xref>,<xref rid="B38-cancers-11-01802" ref-type="bibr">38</xref>]. At the H19/IGF2 locus, Vennin et al. discovered a newly conserved lncRNA antisense to H19 gene—H91 [<xref rid="B39-cancers-11-01802" ref-type="bibr">39</xref>]. H91 promotes IGF2 gene expression through a novel promoter named Pm [<xref rid="B40-cancers-11-01802" ref-type="bibr">40</xref>]. In-vitro and in-vivo studies have established that over-expressed H91 disturbs epigenetic modifications of H19 and IGF2 to promote BC development as an oncogene [<xref rid="B39-cancers-11-01802" ref-type="bibr">39</xref>].</p></sec><sec id="sec2dot1dot3-cancers-11-01802"><title>2.1.3. HOTAIR</title><p>Homeobox transcript antisense RNA (HOTAIR) is closely related to BC size, advancement, and extent of metastasis [<xref rid="B41-cancers-11-01802" ref-type="bibr">41</xref>,<xref rid="B42-cancers-11-01802" ref-type="bibr">42</xref>]. Years ago, it was speculated that HOTAIR might promote tumor aggressiveness through the upregulation of vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) and EMT-related genes [<xref rid="B43-cancers-11-01802" ref-type="bibr">43</xref>]. Knockdown of HOTAIR inhibits the migration and invasion ability of BC cells via the P53/protein kinase B (AKT)/c-Jun N-terminal kinase (JNK)/MMPs signaling pathway [<xref rid="B44-cancers-11-01802" ref-type="bibr">44</xref>] and the AKT/mammalian target of the rapamycin (mTOR) signaling pathway [<xref rid="B45-cancers-11-01802" ref-type="bibr">45</xref>]. Currently, based on the bidirectional interaction between lncRNAs and miRNAs, researchers are trying to investigate more signaling networks involving miRNAs. HOTAIR could act as a sponge for miR-20a-5p and significantly influences migration and invasion through the HOTAIR/miR-20a-5p/high-mobility group AT-hook 2 (HMGA2) axis [<xref rid="B46-cancers-11-01802" ref-type="bibr">46</xref>].</p></sec><sec id="sec2dot1dot4-cancers-11-01802"><title>2.1.4. LINC00152</title><p>LncRNA LINC00152, an 828-bp lncRNA that is located on chromosome 2p11.2, was initially defined as differentially hypomethylated during hepatocarcinogenesis [<xref rid="B47-cancers-11-01802" ref-type="bibr">47</xref>]. LINC00152 is highly expressed in various types of BC tissues, promoting invasion and migration of cancer cells [<xref rid="B48-cancers-11-01802" ref-type="bibr">48</xref>,<xref rid="B49-cancers-11-01802" ref-type="bibr">49</xref>,<xref rid="B50-cancers-11-01802" ref-type="bibr">50</xref>]. With the knockdown of LINC00152, many studies observed inhibited migration and invasion of MDA-MB-231 cells and MCF-7 cells [<xref rid="B49-cancers-11-01802" ref-type="bibr">49</xref>,<xref rid="B50-cancers-11-01802" ref-type="bibr">50</xref>]. In agreement with findings in TNBC cell lines, LINC00152 is highly expressed in TNBC tissues and mechanistically LINC000152 induces tumorigenesis by inactivation of the tumor-suppressive breast cancer gene 1 (BRCA1)/gene of phosphate and tension homology deleted on chromosome ten (PTEN) signaling [<xref rid="B48-cancers-11-01802" ref-type="bibr">48</xref>]. In ER-positive cancer cells, Hu et al. cast light not only on the positive effect of LINC00152 on one of the cellular preconditions for cancer metastasis, EMT, but also on chemo-resistance to doxorubicin (DOX) [<xref rid="B49-cancers-11-01802" ref-type="bibr">49</xref>].</p></sec><sec id="sec2dot1dot5-cancers-11-01802"><title>2.1.5. LINC00461</title><p>LncRNA LINC00461 is a novel tumor promoter in BC and is transcribed from a gene located at an intergenic region of human chromosome 5 [<xref rid="B51-cancers-11-01802" ref-type="bibr">51</xref>]. Over-expression of LINC00461 results in upregulated expression of vimentin, E-cadherin, and ZEB1 [<xref rid="B52-cancers-11-01802" ref-type="bibr">52</xref>,<xref rid="B53-cancers-11-01802" ref-type="bibr">53</xref>,<xref rid="B54-cancers-11-01802" ref-type="bibr">54</xref>]. Additionally, up-regulation of LINC00461 accelerates BC cell migration and invasion through the miR-30a-5p/integrin β3 axis [<xref rid="B53-cancers-11-01802" ref-type="bibr">53</xref>]. These findings provide a basis for the association of LINC000461, EMT, and aggressive phenotypes of human cancer.</p></sec><sec id="sec2dot1dot6-cancers-11-01802"><title>2.1.6. NEAT1</title><p>Transcriptome sequencing and next-generation sequencing files have shown that nuclear-enriched abundant transcript 1 (NEAT1) is one of the highest expressed lncRNAs in BC [<xref rid="B55-cancers-11-01802" ref-type="bibr">55</xref>,<xref rid="B56-cancers-11-01802" ref-type="bibr">56</xref>]. Across the four subtype-related ceRNA networks, NEAT1 has specific roles in each subtype through competing with diverse mRNAs [<xref rid="B56-cancers-11-01802" ref-type="bibr">56</xref>]. These results hint at a strong connection between oncogenic effects of NEAT1 and BC. The latest studies suggest NEAT1 has a crucial role in promoting the growth, migration and invasion capacity of BC cells [<xref rid="B57-cancers-11-01802" ref-type="bibr">57</xref>]. Despite the lack of in-vivo research with clinical BC samples, NEAT1 has been verified as an miR-448 sponge to enhance zinc finger E-Box binding homeobox 1 (ZEB1) expression, and this phenomenon can be reversed by an miR-448 mimic in vitro [<xref rid="B58-cancers-11-01802" ref-type="bibr">58</xref>]. In triple-negative breast cancer, NEAT1 confers oncogenic effects through modulating chemoresistance and cancer stemness [<xref rid="B59-cancers-11-01802" ref-type="bibr">59</xref>].</p></sec><sec id="sec2dot1dot7-cancers-11-01802"><title>2.1.7. LINC01857</title><p>As a sharply up-regulated lncRNA in BC tissue, previous studies have noted that LINC01857 is usually associated with poor prognosis of BC patients [<xref rid="B60-cancers-11-01802" ref-type="bibr">60</xref>]. The cAMP response element-binding protein binding protein (CREBBP) is an acetyltransferase that is commonly considered a tumor suppressor in BC [<xref rid="B61-cancers-11-01802" ref-type="bibr">61</xref>,<xref rid="B62-cancers-11-01802" ref-type="bibr">62</xref>]. Knockdown of LINC01857 inhibits H3K27Ac and cAMP response element-binding protein 1 (CREB1) transcription via reducing the enrichment of CREBBP in the CREB1 promoter region. Overexpression of CREB1 in MCF-7 cells reverses the inhibition effect of LINC01857 knockdown, leading to larger quantities of migration and invasion cells [<xref rid="B60-cancers-11-01802" ref-type="bibr">60</xref>].</p></sec></sec><sec id="sec2dot2-cancers-11-01802"><title>2.2. LncRNAs That Promote Distant Metastasis of BC Cells</title><sec id="sec2dot2dot1-cancers-11-01802"><title>2.2.1. H19</title><p>In 2017, Zhou et al. isolated BC cells from the primary mammary tumor, circulation, and metastatic lesions in the lungs of TA2 mice and found that H19 is an essential key factor in several tumor metastasis procedures. In cells isolated from plasma blood, H19 acts as an endogenous sponge by directly binding to let-7b. Subsequently, the binding of let-7b and cytohesin 3 (CYTH3; one of ArfGEFs) activates adenosine 5′-diphosphate (ADP) ribosylation factor (ARF) and EMT [<xref rid="B63-cancers-11-01802" ref-type="bibr">63</xref>]. Contrarily, in cells isolated from the primary tumor and lung metastasis tumor, H19 regulates GIT2 via sponging miR-200b/c and promotes G protein-coupled receptor kinase interacting protein 2 (GTI2; one of ArfGAPs) expression through inactivating ARF [<xref rid="B63-cancers-11-01802" ref-type="bibr">63</xref>]; thus, MET took place in order to accelerate successful metastatic colonization of a secondary organ [<xref rid="B64-cancers-11-01802" ref-type="bibr">64</xref>,<xref rid="B65-cancers-11-01802" ref-type="bibr">65</xref>]. Matouk et al. revealed in their research that hypoxia-induced EMT is associated with strong induction of both H19 and miR-675, and the H19 gene is highly expressed in common metastatic sites regardless of the tumor’s primary origin [<xref rid="B66-cancers-11-01802" ref-type="bibr">66</xref>]. Therefore, we suggest H19 is a tumor-promoting lncRNA that endows distant metastatic potential to BC cells.</p></sec><sec id="sec2dot2dot2-cancers-11-01802"><title>2.2.2. HOTAIR</title><p>In recent years, HOTAIR has been one of the most well-studied lncRNAs. Alongside invasion and migration of BC cells, HOTAIR participates in metastasis of BC as well. Mounting evidence has revealed the positive correlation between high circulating HOTAIR and lymph node metastasis, as well as distant metastasis of BC [<xref rid="B67-cancers-11-01802" ref-type="bibr">67</xref>].</p><p>Epigenetic signaling from the tumor microenvironment regulates the switch from dormancy to metastatic growth [<xref rid="B68-cancers-11-01802" ref-type="bibr">68</xref>]. Apart from studies focusing on cross talks in the BC cell itself, the latest emerging studies have investigated the roles of lncRNAs in the tumor microenvironment. By establishing an orthotopic mouse model of MDA-MB-231 cells, previous studies have explored a novel transforming growth factor-beta1 (TGF-β1)/cyclin-dependent kinase 5 (CDK5)/HOTAIR/H3K27 signaling that could promote tumor growth, lymph node metastasis, and breast-to-lung metastasis [<xref rid="B69-cancers-11-01802" ref-type="bibr">69</xref>]. Additionally, emerging evidence from laminin-rich extracellular matrix-based three-dimensional organotypic culture (lrECM 3D) has suggested the presence of epigenetic regulation of gene expression by extracellular matrix (ECM) signaling in cancer cells [<xref rid="B70-cancers-11-01802" ref-type="bibr">70</xref>,<xref rid="B71-cancers-11-01802" ref-type="bibr">71</xref>]. Interestingly, HOTAIR expression exhibits robust induction in lrECM 3D over that in 2D culture, and such an induction partly relies on bromodomain containing 4 (BRD4) and the canonical ECM signaling pathway, namely integrins and Src kinase [<xref rid="B72-cancers-11-01802" ref-type="bibr">72</xref>]. This validates the significant observations of Gupta et al., who suggested conventional 2D cultures which lacked critical factors that stimulated the expression of HOTAIR and promoted cancer metastasis very early [<xref rid="B73-cancers-11-01802" ref-type="bibr">73</xref>].</p></sec><sec id="sec2dot2dot3-cancers-11-01802"><title>2.2.3. HIF1A-AS2</title><p>Hypoxia-inducible factor 1 alpha-antisense RNA 2 (HIF1A-AS2) may be a latent tumor promotor in TNBC patients. In vitro, HIF1A-AS2 obviously depresses TNBC cell migration and invasion; in 86 TNBC cases, high expression of HIF1A-AS2 was associated with more lymph node metastasis, distant metastasis, and unfavorable histological grade [<xref rid="B74-cancers-11-01802" ref-type="bibr">74</xref>]. Previous studies have found even higher plasma levels of HIF1A-AS2 expression in BC cases with lymph node metastasis [<xref rid="B75-cancers-11-01802" ref-type="bibr">75</xref>].</p></sec><sec id="sec2dot2dot4-cancers-11-01802"><title>2.2.4. RP1</title><p>Jia et al. first identified a novel lncRNA on chromosome 22 and named it lncRNA RP1. They found that RP1 was significantly upregulated in BC tissue, and RP1 could enhance the metastasis of BC in vitro and in vivo through the Kruppel-like factor 5 (KLF5)/RP1/p27kip1 signaling pathway. Mechanistically, RP1 attenuated p27kip1 translation through interacting with complex p-4E-BP1/eIF4E and restored p27kip1-downregulated Snail1, thus promoting BC progression [<xref rid="B76-cancers-11-01802" ref-type="bibr">76</xref>].</p></sec><sec id="sec2dot2dot5-cancers-11-01802"><title>2.2.5. MALAT1</title><p>The nuclear lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is among the most conserved and highly abundant lncRNAs in normal tissues, suggesting that it may have vital biological implications [<xref rid="B77-cancers-11-01802" ref-type="bibr">77</xref>]. When it comes to BC metastasis, overwhelming previous findings indicate its increased expression is associated with relapse and metastatic progression in BC. Up-regulation of MALAT1 in the tissue and serum of BC, generated by different strategies, has been reported by independent groups [<xref rid="B78-cancers-11-01802" ref-type="bibr">78</xref>,<xref rid="B79-cancers-11-01802" ref-type="bibr">79</xref>,<xref rid="B80-cancers-11-01802" ref-type="bibr">80</xref>]. This is one novel epigenetic mechanism by which MALAT1 facilitates a pro-metastatic phenotype in BC by trans-regulating EEF1A1 [<xref rid="B81-cancers-11-01802" ref-type="bibr">81</xref>]. Li et al. overexpressed MALAT1 and found this promoted lipopolysaccharide (LPS)-induced invasion and metastasis of human and mouse mammary tumor cells [<xref rid="B82-cancers-11-01802" ref-type="bibr">82</xref>]. Moreover, a novel regulation mechanism of MALAT1 in BC cells was presented by more recent research. They suggested that hypoxia might induce the specific chromatin interactions and increases MALAT1 expression as well as its antisense strand TALAM1 in BC cells [<xref rid="B83-cancers-11-01802" ref-type="bibr">83</xref>]. An in-vivo study showed that Malat1<sup>−/−</sup> mice exhibited a significant reduction in lung macrometastases and a significantly decreased metastatic burden. Moreover, knockdown of Malat1 results in mammary tumor differentiation [<xref rid="B84-cancers-11-01802" ref-type="bibr">84</xref>]. Similar conclusions can be drawn from in-vitro and in-vivo studies on TNBC. Knockdown of MALAT1 impaired TNBC growth and metastasis via the miR-1/slug axis [<xref rid="B80-cancers-11-01802" ref-type="bibr">80</xref>] and MALAT1/miR-129-5p axis [<xref rid="B85-cancers-11-01802" ref-type="bibr">85</xref>].</p></sec></sec></sec><sec id="sec3-cancers-11-01802"><title>3. LncRNAs That Attenuate Aggressiveness of BC Cells </title><sec id="sec3dot1-cancers-11-01802"><title>3.1. LncRNAs That Inhibit Invasion and Migration of BC Cells</title><sec id="sec3dot1dot1-cancers-11-01802"><title>3.1.1. GAS5</title><p>Growth arrest-specific 5 (GAS5) is a noncoding gene that was initially isolated from mouse NIH 3T3 cells [<xref rid="B86-cancers-11-01802" ref-type="bibr">86</xref>]. The expression level of GAS5 is significantly lower in BC in younger cases [<xref rid="B87-cancers-11-01802" ref-type="bibr">87</xref>]. Additionally, studies have demonstrated the negative correlation between GAS5 expression and malignancy of different cell lines of BC [<xref rid="B88-cancers-11-01802" ref-type="bibr">88</xref>]. GAS5 could function as an endogenous sponge that sequesters miR-21, resulting in reciprocal repression of miR-21 and GAS5. This interaction relies on the putative miR-21-binding site at exon 4 of GAS5 and the RNA-induced silencing complex (RISC) [<xref rid="B88-cancers-11-01802" ref-type="bibr">88</xref>]. Additionally, GAS5 inhibits TNBC cell invasion through the miR-196a-5p/forkhead box protein O1 (FOXO1)/phosphatidylinositol 3-kinase (PI3K)/AKT axis, which starts with competitive binding of GAS5 to miR-196a-5p [<xref rid="B89-cancers-11-01802" ref-type="bibr">89</xref>].</p></sec><sec id="sec3dot1dot2-cancers-11-01802"><title>3.1.2. MT1JP</title><p>The lncRNA metallothionein 1J pseudogene (MT1JP) is located on chromosome 16 in a cluster that consists of several homologous protein-coding genes in the metallothionein family. It was first reported as a tumor suppressor that modulates the p53 protein expression level, thereby regulating the p53-related signaling pathway [<xref rid="B90-cancers-11-01802" ref-type="bibr">90</xref>]. Decreased MT1JP expression is significantly associated with more lymphatic metastasis and advanced Tumor Node Metastasis (TNM) stage for gastric cancer patients, and in-vitro and in-vivo studies have shown the suppressive role of MT1JP on the migration and invasion of gastric cancer [<xref rid="B91-cancers-11-01802" ref-type="bibr">91</xref>,<xref rid="B92-cancers-11-01802" ref-type="bibr">92</xref>].</p><p>In terms of BC, one recent study presented the first evidence that MT1JP overexpression markedly inhibits invasion and enhances cisplatin sensitivity of BC cells, which is coincident with gastric cancer results. Mechanistically, MT1JP competitively binds to miR-24-3p and inhibits the Wnt/β-catenin signaling pathway [<xref rid="B93-cancers-11-01802" ref-type="bibr">93</xref>]. More importantly, down-regulated MT1JP expression in BC patients indicates a better prognosis.</p></sec><sec id="sec3dot1dot3-cancers-11-01802"><title>3.1.3. NEF</title><p>A considerable number of studies have observed the down-regulated expression of lncRNA-neighboring enhancer of FOXA2 (NEF) as a tumor suppressor in various types of cancers, for instance, cholangiocarcinoma [<xref rid="B94-cancers-11-01802" ref-type="bibr">94</xref>], non-small-cell lung cancer [<xref rid="B95-cancers-11-01802" ref-type="bibr">95</xref>], and hepatocellular carcinoma [<xref rid="B96-cancers-11-01802" ref-type="bibr">96</xref>]. BC is no exception. Previous in-vitro cell experiment results have indicated that NEF might inhibit TNBC cell migration and invasion by downregulating miRNA-155, and overexpression of miRNA-155 significantly attenuates the inhibitory effects of NEF overexpression on cancer cell migration [<xref rid="B97-cancers-11-01802" ref-type="bibr">97</xref>].</p></sec><sec id="sec3dot1dot4-cancers-11-01802"><title>3.1.4. NKILA</title><p>In various cancer types, evidence indicates that TGF-β-induced EMT is nuclear factor kappa-B (NF-κB)-dependent. LncRNA NKILA is a newly discovered lncRNA that functions as a tumor suppressor in BC metastasis [<xref rid="B98-cancers-11-01802" ref-type="bibr">98</xref>,<xref rid="B99-cancers-11-01802" ref-type="bibr">99</xref>]. In BC, recent research has linked the negative feedback regulation of lncRNA NKILA with NF-κB activation and TGF-β-induced EMT, thus indicating NKILA may inhibit the breast EMT process of BC cells, thus retarding metastasis. Mechanistically, NKILA can suppress several NF-κB target genes by directly binding to the NF-κB/IκB complex [<xref rid="B100-cancers-11-01802" ref-type="bibr">100</xref>]. Furthermore, there is a positive correlation between NKILA and E-cadherin expression level, and the long-term survival of BC patients [<xref rid="B99-cancers-11-01802" ref-type="bibr">99</xref>].</p></sec><sec id="sec3dot1dot5-cancers-11-01802"><title>3.1.5. LET</title><p>LncRNA LET is a newly discovered molecule involved in the invasion and migration of BC. Despite the overall expression of LET in BC tissue and cell lines being down-regulated, LET expression differs in various BC cell lines. LET expression is lower in MDA-MB-231 (BC cell line, triple negative) than MCF-10 (non-tumorigenic epithelial breast cell line), which suggests the negative association between the LET expression level and the acquisition of tumorigenesis abilities of BC cells. Additionally, over-expressing LET increases E-cadherin and decreases N-cadherin and vimentin expression, and thereby represses EMT of BC cells [<xref rid="B101-cancers-11-01802" ref-type="bibr">101</xref>].</p></sec><sec id="sec3dot1dot6-cancers-11-01802"><title>3.1.6. TFAP2A-AS1</title><p>Transcription factor AP-2 alpha-antisense RNA 1 (TFAP2A-AS1) may be a novel tumor suppressor in BC. Transwell assay showed a remarkable decrease of invasive cell numbers in MCF-7 and MDA-MB-231 cells transfected with TFAP2A-AS1. Mechanistically, TFAP2A-AS1 sequesters the miR-933-inhibiting Smad signaling pathway by downregulating drosophila mothers against decapentaplegic family member 2 (SMAD2). An in-vivo study showed that TFAP2A-AS1-overexpressed MCF-7 cells injected in nude mice ended up with a significantly smaller tumor volume and weight [<xref rid="B102-cancers-11-01802" ref-type="bibr">102</xref>].</p></sec><sec id="sec3dot1dot7-cancers-11-01802"><title>3.1.7. LncKLHDC7B </title><p>With knockdown of LncKLHDC7B, Beltran-Anaya et al. confirmed an inverse association between the unique LncKLHDC7B overexpression and migration and invasion in the immunomodulatory subtype of TNBC [<xref rid="B103-cancers-11-01802" ref-type="bibr">103</xref>]. However, they did not investigate the potential mechanism further. To understand the clinical implications of LncKLHDC7B expression, they analyzed public data in 2012 and 2016 [<xref rid="B104-cancers-11-01802" ref-type="bibr">104</xref>,<xref rid="B105-cancers-11-01802" ref-type="bibr">105</xref>,<xref rid="B106-cancers-11-01802" ref-type="bibr">106</xref>] and found that lower LncKLHDC7B expression was related to lower survival and an increased risk of a recurrent or metastatic event.</p></sec></sec><sec id="sec3dot2-cancers-11-01802"><title>3.2. LncRNAs That Inhibit Distant Metastasis of BC Cells</title><sec id="sec3dot2dot1-cancers-11-01802"><title>3.2.1. MALAT1</title><p>On the one hand, as we discussed before, increased expression of MALAT1 is associated with relapse and metastatic progression in breast cancer. On the other hand, a few studies surprisingly provide new insight into MALAT1 as a metastasis-suppressing lncRNA in BC. Several studies have found down-regulated expression of MALAT1 in BC [<xref rid="B107-cancers-11-01802" ref-type="bibr">107</xref>,<xref rid="B108-cancers-11-01802" ref-type="bibr">108</xref>]. Kwok et al. suggested that the PTEN-microRNA-MALAT1 axis may promote tumorigenesis and demonstrated the first evidence that MALAT1 possesses novel tumor-suppressive capabilities in BC [<xref rid="B109-cancers-11-01802" ref-type="bibr">109</xref>]. A similar case was found by establishing both genetically engineered mouse models and xenograft models; Kim et al. observed that metastasis was specifically induced by somatic knockout of Malat1. Mechanistically, MALAT1 prevents prometastatic transcription factor TEA domain family member 2 (TEAD) from associating with its co-activator Yes-associated protein (YAP) [<xref rid="B107-cancers-11-01802" ref-type="bibr">107</xref>].</p><p>Collectively, we cannot conclude whether MALAT1 is a tumor-promoting or suppressing lncRNA; numerous looping events remain to be discovered to explore the possible explanation for the dual effects of MALAT1 in BC.</p></sec><sec id="sec3dot2dot2-cancers-11-01802"><title>3.2.2. MEG3</title><p>LncRNA maternally expressed gene 3 (MEG3) has been implicated in tumorigenesis and progression of BC, and the mechanisms in most cases are associated with DNMT of MEG3. It has been demonstrated that miR-506 could target DNMT1 and DNMT3b to retard tumor development [<xref rid="B110-cancers-11-01802" ref-type="bibr">110</xref>]. Downregulating miR-506 increases the methylation level of MEG3 promoter and inhibits MEG3 expression via the miR-506/SP3/SP1/DNMT1/MEG3 axis in human BC cell lines, resulting in attenuation of metastasis of MCF-7 and MDA-MB-231 cells [<xref rid="B111-cancers-11-01802" ref-type="bibr">111</xref>]. Accordingly, it is plausible to speculate that both miR-506 and MEG3 function as tumor suppressors in BC, which is coincident with previous results [<xref rid="B112-cancers-11-01802" ref-type="bibr">112</xref>,<xref rid="B113-cancers-11-01802" ref-type="bibr">113</xref>]. Additionally, treatment of DNA methylation inhibitor (5′-Aza-2′-deoxycytidine) may partly reverse the signaling and retard tumor development [<xref rid="B114-cancers-11-01802" ref-type="bibr">114</xref>].</p></sec><sec id="sec3dot2dot3-cancers-11-01802"><title>3.2.3. NLIPMT</title><p>Jiang et al. identified a hitherto uncharacterized lncRNA called novel lncRNA, inhibiting proliferation and metastasis (NLIPMT) in BC. An in-vitro study and xenograft study showed that over-expression of NLIPMT inhibited cell motility, growth, and metastasis of BC. Mechanistically, downregulated NLIPMT accelerated proliferation and restored motility of BC cells by promoting the expression of glycogen synthase kinase 3β (GSK3β) and EMT proteins [<xref rid="B115-cancers-11-01802" ref-type="bibr">115</xref>]. Interestingly, according to previous studies, GSK3β has dual effects in different types of cancer. On the one hand, evidence indicates that GSK3β functions as a tumor suppressor in the breast [<xref rid="B116-cancers-11-01802" ref-type="bibr">116</xref>,<xref rid="B117-cancers-11-01802" ref-type="bibr">117</xref>,<xref rid="B118-cancers-11-01802" ref-type="bibr">118</xref>]. On the other hand, a tumor-promoting effect of GSK3β has been indicated in colon [<xref rid="B119-cancers-11-01802" ref-type="bibr">119</xref>] and pancreatic cancers [<xref rid="B120-cancers-11-01802" ref-type="bibr">120</xref>]. Therefore, the conflict of GSK3β’s functions might disturb the effect of NLIPMT in different types of cancer.</p></sec><sec id="sec3dot2dot4-cancers-11-01802"><title>3.2.4. XIST</title><p>The lncRNA X inactive specific transcript (XIST) is a potential tumor suppressor in cancer [<xref rid="B121-cancers-11-01802" ref-type="bibr">121</xref>,<xref rid="B122-cancers-11-01802" ref-type="bibr">122</xref>]. A luciferase reporter assay verified that XIST targets the miR-155/CDX1 axis, and overexpression of XIST remarkably inhibits BC cell migration and invasion [<xref rid="B123-cancers-11-01802" ref-type="bibr">123</xref>]. Xing et al. demonstrated how the overexpression of XIST in BC cells significantly attenuates its metastatic ability to the brain from two different aspects. Firstly, a pathway screening based on gene set enrichment analysis (GSEA) uncovered that XIST activates the c-Met signaling pathway by activation of moesin (MSN) on the X chromosome. MSN, a member of the ERM (ezrin, radixin, and moesin) protein family, participates in the maintenance of epithelial integrity [<xref rid="B124-cancers-11-01802" ref-type="bibr">124</xref>]. Loss of c-Met decreases the transmigration abilities of BC cells and suppresses the breast-to-brain metastatic abilities in vivo [<xref rid="B125-cancers-11-01802" ref-type="bibr">125</xref>]. Secondly, considering activated microglia can modulate neurodegenerative diseases and tumor progression under pathological conditions [<xref rid="B126-cancers-11-01802" ref-type="bibr">126</xref>], they also investigated the role of XIST in microglia. Interestingly, XIST-downregulated BC cells could secrete exosomal miR-503 to reprogram microglia from the M1 (tumor-suppressive) into the M2 (tumor-promoting) phenotype, causing local immune suppression [<xref rid="B125-cancers-11-01802" ref-type="bibr">125</xref>].</p></sec></sec></sec><sec id="sec4-cancers-11-01802"><title>4. The Regulation of LncRNAs in the Stemness of BC Cells</title><p>The cancer stem cell theory indicates that cancers are sustained by tumor-initiating cells, and researchers initially termed these cancer stem cells, with distinct phenotypes and a high tumorigenic potential [<xref rid="B127-cancers-11-01802" ref-type="bibr">127</xref>]. CSCs are the “seeds” of tumor metastasis and recurrence, and have a limitless and high invasion and migration capacity [<xref rid="B128-cancers-11-01802" ref-type="bibr">128</xref>]. The subpopulation of CSCs will express specific biomarkers, giving rise to metastasis; therapy resistance; and the recurrence of cancers such as CD 26, CD133 and CD44v6 [<xref rid="B129-cancers-11-01802" ref-type="bibr">129</xref>,<xref rid="B130-cancers-11-01802" ref-type="bibr">130</xref>].</p><p>Currently, with further research emerging on lncRNAs, many researchers have suggested that lncRNAs are required for stemness maintenance of cancer cell lines [<xref rid="B131-cancers-11-01802" ref-type="bibr">131</xref>]. However, whether and how lncRNAs have a role in breast cancer stem-like cells (BCSCs) remains unclear. Discussing the potential mechanism of lncRNA function may contribute to developing novel therapeutic approaches. Herein, we review our current understanding of the cell-biological mechanisms that regulate BC metastasis, with BCSCs and lncRNAs as the pivotal objects.</p><p>EMT is a cellular process that is not only strongly correlated with tumor metastasis, but also with CSC [<xref rid="B132-cancers-11-01802" ref-type="bibr">132</xref>]. LncRNAs have been demonstrated to play vital roles during EMT, and some of these molecules also have regulatory roles in the proliferation of CSC [<xref rid="B133-cancers-11-01802" ref-type="bibr">133</xref>], although their functions are still unclear in BC. Current research indicates that T-cell leukemia 1 upstream neural differentiation-associated RNA (TUNAR, LINC00617) functions as a vital promotor of EMT and causes generation of stem cell properties via activating the transcription of SOX2, thus promoting BC progression and metastasis [<xref rid="B134-cancers-11-01802" ref-type="bibr">134</xref>]. LncRNA ES1 (LINC01108) and a hedgehog pathway-associated lncRNA called lncRNA-Hh can enhance the stem cell properties of BC via regulating SOX2 as well [<xref rid="B135-cancers-11-01802" ref-type="bibr">135</xref>,<xref rid="B136-cancers-11-01802" ref-type="bibr">136</xref>]. ES1 controls the expression of stemness transcription factors in BC cells by regulating the OCT4/SOX2/miR-302 axis [<xref rid="B135-cancers-11-01802" ref-type="bibr">135</xref>]; lncRNA-Hh directly targets GAS1 to increase the SOX2 and OCT4 expression, thus promoting the CSCs-like characteristics of Twist-driven EMT cells and Twist-positive BC cells [<xref rid="B136-cancers-11-01802" ref-type="bibr">136</xref>]. LncRNAs could also attenuate stemness in BC cells via inhibiting EMT. The study on brain metastasis of BC found that the lncRNA XIST suppressed EMT and the MSN/c-Met axis via MSN-mediated protein stabilization, which leads to the attenuation of stemness in the tumor cells. The negative correlation between RNA of XIST and c-Met expression was also observed in brain metastasis samples from BC patients [<xref rid="B125-cancers-11-01802" ref-type="bibr">125</xref>].</p><p>LncRNAs can regulate oncogenic transcription factor in stemness properties via sponging miRNAs as a ceRNA. HOTAIR could suppress miR-34a, resulting in remarkably up-regulated SOX2, P53, self-renewal capacity, and migration of CSC-MCF7 [<xref rid="B137-cancers-11-01802" ref-type="bibr">137</xref>]. Apart from HOTAIR, FEZ family zinc finger 1-antisense 1 (FEZF1-AS1) and LINC00511 can promote the BCSC properties via FEZF1-AS1/miR-30a/Nanog and the LINC00511/miR-185-3p/E2F1/Nanog signaling pathway, respectively [<xref rid="B138-cancers-11-01802" ref-type="bibr">138</xref>,<xref rid="B139-cancers-11-01802" ref-type="bibr">139</xref>]. Contrarily, the tumor-suppressive lncRNA fibroblast growth factor 13-antisense RNA 1 (FGF13-AS1) could act as an endogenous sponge by directly binding to Myc mRNA via binding insulin-like growth factor 2 mRNA binding proteins (IGF2BP), followed by the obstructive combination of IGF2BPs and Myc mRNA [<xref rid="B140-cancers-11-01802" ref-type="bibr">140</xref>]. Myc is an oncogenic transcription factor that plays vital roles in glycolysis and stemness properties [<xref rid="B141-cancers-11-01802" ref-type="bibr">141</xref>]. Furthermore, a feedback loop between Myc and FGF13-AS1 also participates in regulating these novel suppressive effects of FGF13-AS1 [<xref rid="B141-cancers-11-01802" ref-type="bibr">141</xref>]. Impaired function of Myc may explain how FGF13-AS1-inhibited BC cells achieve migration and invasion.</p><p>In addition to the effect of lncRNA dysregulation on EMT proteins and oncogenic transcription factors in stemness properties, the latest studies point out that lncRNAs play a role in BCSC maintenance under hypoxia via the tricarboxylic acid cycle [<xref rid="B142-cancers-11-01802" ref-type="bibr">142</xref>]. Mechanistically, H19 sequesters miRNA let-7 as a ceRNA, leading to hypoxia-inducible factor-1α (HIF-1α) release and an increase in pyruvate dehydrogenase kinase 1 (PDK1) expression [<xref rid="B143-cancers-11-01802" ref-type="bibr">143</xref>]. PDK1, an essential glycolytic enzyme, is correlated with tumor proliferation, metastasis, and poor prognosis [<xref rid="B144-cancers-11-01802" ref-type="bibr">144</xref>,<xref rid="B145-cancers-11-01802" ref-type="bibr">145</xref>]. Therefore, it is plausible to conclude that H19 may activate PDK1 in BCSC via the let-7/HIF-1 axis under hypoxia, and this mechanism may be required in the development of primary breast carcinomas.</p></sec><sec id="sec5-cancers-11-01802"><title>5. The Regulation of LncRNAs in the Angiogenesis in BC</title><p>Angiogenesis refers to the process of neovessels sprouting from preexisting vessels, as opposed to the vasculogenesis of embryonic fibroblasts and their consequently activating proliferation, invasion, and metastasis of cancer cells [<xref rid="B146-cancers-11-01802" ref-type="bibr">146</xref>]. It is well known that the more pathological angiogenesis occurs, the more chances for cancer cells to migrate into the circulatory system and achieve distant metastasis. However, during the last few years, despite many reviews aimed at organizing the mechanism underneath BC angiogenesis, only a few reviews have associated BC angiogenesis with lncRNAs. Here, we review how lncRNAs participate in the angiogenesis of BC, thus further supporting the understanding of their involvement in promoting or inhibiting BC metastasis.</p><p>LncRNA MALAT1 is considered an oncogenic regulator of BC, and we have discussed its role in regulating the aggressiveness of BC cells. Vascular endothelial growth factor (VEGF) is the crucial signaling molecule for angiogenesis, acting by regulating proliferation, survival, and migration of the cancer [<xref rid="B147-cancers-11-01802" ref-type="bibr">147</xref>]. In terms of BC angiogenesis, up-regulated MALAT1 in BC tissue also shows oncogenic effects in vitro and in vivo through VEGF regulation. Mechanistically, knockdown of MALAT1 significantly promotes angiogenesis of BC through upregulating the expression level of miR-145 in MCF-7 cells and BC tissue [<xref rid="B148-cancers-11-01802" ref-type="bibr">148</xref>].</p><p>Some tumor-suppressive lncRNAs also exhibit negative regulatory effects on BC angiogenesis. For example, MEG3 not only inhibits the aggressiveness of BC cells, but also inhibits BC angiogenesis via regulating the VEGF or AKT pathway [<xref rid="B149-cancers-11-01802" ref-type="bibr">149</xref>,<xref rid="B150-cancers-11-01802" ref-type="bibr">150</xref>].</p></sec><sec id="sec6-cancers-11-01802"><title>6. The Regulation of LncRNAs in Chemotherapy Resistance in BC</title><p>The current clinical treatments for BC patients include surgery and postoperative chemotherapy, targeted therapy, or radiation therapy [<xref rid="B151-cancers-11-01802" ref-type="bibr">151</xref>]. It is critical to select the chemotherapy regimens wisely, because different types of BC will respond to different regiments and specific drugs. For example, ribociclib plus fulvestrant (hormone receptor-positive/HER-2+) [<xref rid="B152-cancers-11-01802" ref-type="bibr">152</xref>]; trastuzumab, neratinib and lapatinib (HER-2+) [<xref rid="B153-cancers-11-01802" ref-type="bibr">153</xref>,<xref rid="B154-cancers-11-01802" ref-type="bibr">154</xref>]; or ipatasertib plus paclitaxel (TNBC) [<xref rid="B155-cancers-11-01802" ref-type="bibr">155</xref>]. Working on distinct molecular mechanisms, these chemotherapies act synergistically and eliminate most tumor cells during the initial treatment phase. However, the frequent development of drug resistance is still a major obstacle for medical personnel and BC patients. BC recurrences continued to occur steadily throughout the study period from 5 to 20 years, with risks ranging from 10% to 41% [<xref rid="B156-cancers-11-01802" ref-type="bibr">156</xref>]. This emphasizes the urgent need for deeper insight into the molecular mechanisms leading to therapy resistance, especially chemotherapy resistance.</p><p>It is well established that EMT is not only associated with tumor metastasis and cancer cell stemness, but also with resistance to conventional therapies [<xref rid="B6-cancers-11-01802" ref-type="bibr">6</xref>]. Chemotherapy-resistant cells treated by chemotherapeutics (e.g., oxaliplatin, 5-fluorouracil) undergo EMT, and this applies to cells treated with monoclonal antibodies (e.g., trastuzumab) as well [<xref rid="B157-cancers-11-01802" ref-type="bibr">157</xref>]. As outlined in previous sections, it is well established that several lncRNAs play crucial roles in the aggressiveness of BC. Next, we are going to review lncRNAs in participating signaling pathways that modulate both the aggressiveness and chemotherapy resistance of BC cells.</p><p>BC cells that undergo EMT usually show resistance to 5-fluoroutacil (5-FU) treatment [<xref rid="B158-cancers-11-01802" ref-type="bibr">158</xref>]. Knockdown of NEAT1 sensitizes TNBC cells to chemotherapy, indicating its involvement in chemotherapy resistance [<xref rid="B59-cancers-11-01802" ref-type="bibr">59</xref>]. Mechanistically, in-vitro and in-vivo studies have shown that NEAT1 promotes distant metastasis and 5-FU resistance through the miR-129/ZEB2 axis and miR-211/HMGA2 axis in BC [<xref rid="B159-cancers-11-01802" ref-type="bibr">159</xref>,<xref rid="B160-cancers-11-01802" ref-type="bibr">160</xref>]. Similarly, up-regulated terminal differentiation-induced non-coding RNA (TINCR) significantly promotes EMT-associated protein expression and HER-2 expression in trastuzumab-resistant BC cells via the miR-125b-HER-2/Snail-1 signaling pathway [<xref rid="B157-cancers-11-01802" ref-type="bibr">157</xref>].</p><p>Wnt/β-catenin signaling is one of the well-established signaling pathways that regulates EMT in various cancer types. LncRNAs regulating aggressive cytology of cancer cells via the Wnt/β-catenin signaling pathway have been reviewed before [<xref rid="B161-cancers-11-01802" ref-type="bibr">161</xref>]. Several novel lncRNAs may regulate chemotherapy resistance through regulating Wnt/β-catenin signaling. LINC00968 is a newly discovered lncRNA that has suppressive roles in cancer progression [<xref rid="B162-cancers-11-01802" ref-type="bibr">162</xref>]. LINC00968 can attenuate drug resistance of MCF-7/ADM and KPL-4/ADM cells to adriamycin, taxel, and vincristine. Mechanistically, LINC00968 inhibits the Wnt2/β-catenin signaling pathway via hairy/enhancer-of-split related with YRPW motif 1 (HEY1) [<xref rid="B163-cancers-11-01802" ref-type="bibr">163</xref>]. Additionally, knockdown of lncRNA UCA1 increases the tamoxifen sensitivity of BC cells via inhibition of the Wnt/β-catenin pathway.</p><p>Differently to the lncRNAs above that were correlated with EMT, the lncRNA in the non-homologous end-joining pathway 1 (LINP1) is overexpressed in drug-resistant cells and mediates its oncogenic role in BC by decreased apoptosis-related proteins (such as caspase-8 and caspase-9), thus promoting cell growth, metastasis, and chemotherapy resistance to 5-FU and DOX in BC [<xref rid="B164-cancers-11-01802" ref-type="bibr">164</xref>]. 5-FU and DOX are two effective and crucial chemotherapeutics against BC [<xref rid="B165-cancers-11-01802" ref-type="bibr">165</xref>], which can interact with DNA by hindering macro-molecular biosynthesis [<xref rid="B166-cancers-11-01802" ref-type="bibr">166</xref>].</p><p>Taken together, the studies above have revealed a new role for lncRNAs in elucidating the epigenetic mechanism of chemo-resistance. Mechanistically, most lncRNAs are recognized as involved in EMT to amplify or attenuate BC cell response to chemotherapy, and among them, Wnt/β-catenin signaling is a crucial common pathway. LncRNA-regulated apoptosis of BC cells also has an additional effect on chemotherapy resistance to 5-FU and DOX. However, more tissue samples and animal models are required to further investigate the correlation between associated lncRNA expression and patient clinicopathological features, in order to evaluate the potential of lncRNAs as independent biomarkers in BC.</p></sec><sec sec-type="subjects" id="sec7-cancers-11-01802"><title>7. LncRNAs That Function as Prognostic Biomarkers for BC Patients</title><sec id="sec7dot1-cancers-11-01802" sec-type="subjects"><title>7.1. LncRNAs as Prognostic Biomarkers for BC Patients</title><p>As we reviewed above, MALAT1 could be either a metastasis promoter or suppressor in BC patients. In terms of prognosis, current research approves of the association between over-expression of MALAT1 and poor prognosis in BC patients. Meta-analysis indicated that upregulated expression of MALAT1 in BC tissues is significantly associated with more lymph node metastasis, shorter 5-year adverse disease-free survival (DFS) and shorter overall survival (OS) [<xref rid="B167-cancers-11-01802" ref-type="bibr">167</xref>]. Interestingly, MALAT1 was also an important pro-inflammatory factor regulating lipopolysaccharide-induced inflammatory responses in endothelial cells of BC. Li et al. found that MALAT1 was elevated in BC patients with postoperative fever, and high expression of MALAT1 predicted adverse short-term recurrence-free survival (RFS) [<xref rid="B82-cancers-11-01802" ref-type="bibr">82</xref>]. Additionally, an upregulated MALAT1 expression level was related to positive progesterone receptor (PR) status. This might be coincident with the dual role of MALAT1 in BC [<xref rid="B167-cancers-11-01802" ref-type="bibr">167</xref>].</p><p>Many studies have illustrated the tumor-promoting role of HOTAIR in BC progression and the association between over-expression of HOTAIR in tissues and shorter survival in BC patients [<xref rid="B168-cancers-11-01802" ref-type="bibr">168</xref>]. Of particular note, the Kaplan-Meier survival curve showed that patients with high circulating HOTAIR expression had a worse DFS than those with low circulating HOTAIR [<xref rid="B67-cancers-11-01802" ref-type="bibr">67</xref>]. Similarly, plasma H19 levels were significantly correlated with lymph node metastasis, and high plasma H19 levels were significantly reversed in postoperative samples [<xref rid="B169-cancers-11-01802" ref-type="bibr">169</xref>]. In addition, analysis in the preoperative and postoperative plasma samples showed the postoperative levels of circulating GAS5 and H19 significantly decreased, and circulating GAS5 levels in the patients with a positive lymph node metastasis state decreased after surgery [<xref rid="B170-cancers-11-01802" ref-type="bibr">170</xref>]. Therefore, circulating HOTAIR, H19 and GAS5 could be potential biomarkers for BC early screening and prognosis monitoring.</p><p>In addition, as shown in <xref ref-type="fig" rid="cancers-11-01802-f001">Figure 1</xref>, the expression of LINC00473 [<xref rid="B171-cancers-11-01802" ref-type="bibr">171</xref>], TINCR [<xref rid="B157-cancers-11-01802" ref-type="bibr">157</xref>], LINP1 [<xref rid="B172-cancers-11-01802" ref-type="bibr">172</xref>] and lncRNA breast cancer anti-estrogen resistance 4 (BCAR4) [<xref rid="B173-cancers-11-01802" ref-type="bibr">173</xref>,<xref rid="B174-cancers-11-01802" ref-type="bibr">174</xref>] were all up-regulated in BC tissues and increased further during metastasis, and they were all associated with poor prognosis of BC patients. Of particular note, the over-expression of BCAR4 was not only negatively correlated with OS in BC patients, but was also highly correlated with the incidence of BC, so it might be applied as a major negative and unfavorable prognostic marker for BC [<xref rid="B173-cancers-11-01802" ref-type="bibr">173</xref>,<xref rid="B174-cancers-11-01802" ref-type="bibr">174</xref>].</p></sec><sec id="sec7dot2-cancers-11-01802" sec-type="subjects"><title>7.2. LncRNAs as Biomarkers for Diagnosis and Prognosis of TNBC Patients</title><p>Due to the lack of effective targeted therapies and high recurrence rate in response to chemotherapy, the prognosis of TNBC is the most unfavorable among all types of BC. It is therefore urgent to identify the prognostic biomarkers for the diagnosis of TNBC, or its individualized therapy targets.</p><p>In 2016, through detecting the expression levels of lncRNAs in TNBC and non-TNBC tissues separately, Lv et al. identified four lncRNAs (RP11-434D9.1, LINC00052, BC016831, and immunoglobulin kappa variable (IGKV)) as biomarkers to differentiate TNBC cancer from non-TNBC [<xref rid="B175-cancers-11-01802" ref-type="bibr">175</xref>]. As shown in <xref ref-type="fig" rid="cancers-11-01802-f002">Figure 2</xref>, we reviewed the latest studies that revealed lncRNAs as novel prognostic biomarkers for TNBC patients in particular.</p><p>Some tumor-promoting lncRNAs in TNBC may function as biomarkers for diagnosis and prognosis of TNBC patients. Collation of research on 63 TNBC tissues showed DANCR expression was abruptly upregulated and correlated with worse OS and TNM stages [<xref rid="B27-cancers-11-01802" ref-type="bibr">27</xref>]. By utilizing The Cancer Genome Atlas (TCGA) database and analyzing clinical TNBC samples, Zhang et al. found that the expression of nicotinamide phosphoribosyltransferase antisense RNA (NAMPT-AS) was up-regulated, which epigenetically activates NAMPT to promote tumor progression and metastasis [<xref rid="B176-cancers-11-01802" ref-type="bibr">176</xref>]. In addition, according to Kaplan-Meier survival curve analysis, up-regulated expression levels of lncRNA-ATB, NAMPT-AS and HIF1A-AS2 are negatively correlated with OS and DFS of TNBC patients [<xref rid="B74-cancers-11-01802" ref-type="bibr">74</xref>,<xref rid="B176-cancers-11-01802" ref-type="bibr">176</xref>,<xref rid="B177-cancers-11-01802" ref-type="bibr">177</xref>].</p><p>Further, some tumor-suppressive lncRNAs in TNBC may function as biomarkers for diagnosis and prognosis of TNBC patients as well. For example, the latest study observed that TNBC patients with low miR-503 host gene (MIR503HG) expression had a significantly worse prognosis compared with those with high MIR503HG expression, and low MIR503HG expression was a poor independent prognostic factor for OS in TNBC patients [<xref rid="B178-cancers-11-01802" ref-type="bibr">178</xref>].</p><p>In summary, the clinical function of lncRNA is a topic of interest nowadays, including how they can be used for predicting prognosis or serving as therapeutic targets. However, existing research is not sufficient to support clinical applications, and the underlining clinical relevance of lncRNAs and BC still awaits for future validation. Our review aims to provide direction for further research in the future to promote better clinical practice applications.</p></sec></sec><sec sec-type="discussion" id="sec8-cancers-11-01802"><title>8. Discussion</title><p>BC is an aggressive malignant disease in women worldwide, with a high tendency to metastasize [<xref rid="B1-cancers-11-01802" ref-type="bibr">1</xref>]. Novel lncRNA discoveries and the increasing quality of lncRNA function studies are providing new ideas to improve understanding of the mechanism of BC pathogenesis and progression. It has been demonstrated that many lncRNAs have crucial roles in the cell proliferation of BC [<xref rid="B179-cancers-11-01802" ref-type="bibr">179</xref>]. Despite the fact that BC is at the forefront of cancer research, very few studies had investigated the association between lncRNAs and BC distant metastasis until the last 5 years.</p><p>Here, we have reviewed the latest findings of how lncRNAs participate in BC progression, especially metastasis ability. Many researchers have tried to cast light on signaling pathways involved in the metastasis of BC. As shown in <xref rid="cancers-11-01802-t001" ref-type="table">Table 1</xref>, we summarize the mechanisms of different processes that are necessary for metastasis to take place.
<list list-type="bullet"><list-item><p>LncRNAs participate in regulating the aggressiveness of BC cells (such as HOTAIR, H19, DANCR, RP1, GAS5, LNC00152, NEF, and NKILA).</p></list-item><list-item><p>LncRNAs can regulate the stemness properties of BC cells (such as HOTAIR, H19, ES1, TUNAR, lncRNA-Hh, XIST, and FEZF1-AS1).</p></list-item><list-item><p>LncRNAs can regulate angiogenesis of BC (such as MALAT1, MEG3, and LINC00968).</p></list-item></list></p><p>In the next section, we briefly review lncRNAs that can regulate the sensitivity to chemotherapy in vitro and in vivo, and some may function as biomarkers to diagnosis or predict prognosis for BC patients (such as HOTAIR, H19, MALAT1, TINCR, LINC00473, LINP1, BCAR4, and SNHG6).</p><p>Interestingly, we found that some particular lncRNAs have dual effects in BC, indicated by opposite previous findings and conclusions; for example, different research provided almost opposite evidence for the roles of MALAT1 in BC. Of note, there exist some differences in the materials and design of these experiments; for example, Kim et al. suggested MALAT1 was a suppressor by conducting experiments on MCF10A and MDA-MB-231 cells [<xref rid="B107-cancers-11-01802" ref-type="bibr">107</xref>]. Arun et al. report that genetic loss or systemic knockdown of Malat1 results in slower tumor growth accompanied by significant differentiation into cystic tumors and a reduction in metastasis [<xref rid="B84-cancers-11-01802" ref-type="bibr">84</xref>]. Additionally, Li et al. suggested MALAT1 might promote recurrence and lung metastasis of BC patients with early postoperative fever by analyzing plasma levels of MALAT1 in 258 cases of patients with primary breast carcinoma, and knock down of MALAT1 in 4T1 xenograft mice [<xref rid="B82-cancers-11-01802" ref-type="bibr">82</xref>]. Therefore, the foremost cause of the discrepancy may be due to the tumor microenvironment (TME) and metabolism of lncRNA in vivo, and clearly further work needs to be performed to establish whether MALAT1 does have dual effects in BC.</p><p>The intimate association between EMT and CSCs has provided further insights into tumor progression and the contribution of CSCs to tumor metastasis and colonization. Interestingly, most studies on CSC and EMT center on the epigenetic differences between CSCs and non-stem cancer cells, while irreversible mutations in genes can also endow cells with metastasis ability. For example, gene-specific cell cloning in pancreatic cancer and medulloblastoma causes tumor metastasis [<xref rid="B181-cancers-11-01802" ref-type="bibr">181</xref>,<xref rid="B182-cancers-11-01802" ref-type="bibr">182</xref>]. This unexpected phenomenon raises a question: Is it that only CSC can lead to metastasis through genetic changes, or can non-stem cancer cells acquire tumorigenesis and metastasis at the same time via genetic changes? This question still needs in-situ cancer formation experiments to find an answer.</p><p>Autophagy is a rather conservative biological process, regulated by autophagy-related genes (ATGs) [<xref rid="B183-cancers-11-01802" ref-type="bibr">183</xref>]. In this process, eukaryotic organelles and various substances form autophagosomes in the phospholipid bilayer; subsequently, autophagosomes go through degradation and recycling after transporting to the lysosomes. Some state that autophagy is a double-edge-sword for tumor metastasis. On the one hand, it reduces tumor necrosis induced by hypoxia, inhibits the infiltration of inflammatory cells, and thus inhibits tumor metastasis [<xref rid="B184-cancers-11-01802" ref-type="bibr">184</xref>]. On the other hand, in the early stages of metastasis, autophagy accelerates tumor metastasis through promoting the survival of cells under metabolic stress and oxygen-deficient conditions [<xref rid="B185-cancers-11-01802" ref-type="bibr">185</xref>]. Some have investigated whether lncRNAs function as regulators in BC cells autophagy. Both in-vitro and in-vivo studies indicate that the lncRNA GAS5 facilitates autophagy of BC cells. GAS5 can regulate the expression of ATG3 via the GAS5-miR-23a-ATG3 axis, not only in MDA-MB-231 and MCF-7 cells, but also in patients with BC [<xref rid="B186-cancers-11-01802" ref-type="bibr">186</xref>].</p><p>Some consider that autophagy can promote tumor metastasis by reducing anoikis of cancer cells [<xref rid="B187-cancers-11-01802" ref-type="bibr">187</xref>]. Anoikis refers to programmed apoptosis after separation from ECM [<xref rid="B188-cancers-11-01802" ref-type="bibr">188</xref>]. The anoikis prevention of detached malignant cancer cells is the precondition for metastasis, and an elevated threshold for anoikis usually leads to heightened metastatic potential [<xref rid="B189-cancers-11-01802" ref-type="bibr">189</xref>]. Currently, more and more studies are investigating the role of lncRNAs in cancer cell anoikis. For example, in thyroid carcinoma, lncRNA FOXD2 adjacent opposite strand RNA 1(FOXD2-AS1) promotes the cancer stem cell features and anoikis resistance in thyroid cancer cells via inhibiting the miR-7-5p/telomerase reverse transcriptase (TERT) axis [<xref rid="B190-cancers-11-01802" ref-type="bibr">190</xref>]. In ovarian cancer, caspase 3/7 assay showed that MALAT1 knockdown resulted in increased anoikis [<xref rid="B191-cancers-11-01802" ref-type="bibr">191</xref>]. Similarly, in bladder cancer, knockdown of LINC00958 attenuated resistance to anoikis [<xref rid="B192-cancers-11-01802" ref-type="bibr">192</xref>]. However, as of the time of writing, no research has revealed how lncRNAs function in the anoikis of BC cells. We consider that this may be a promising area for future research.</p><p>In five breast cancer subtypes (luminal A, luminal B, HER2-overexpressing, basal-like, and normal-like), the pathological characteristics and prognostics exhibit significant differences [<xref rid="B193-cancers-11-01802" ref-type="bibr">193</xref>,<xref rid="B194-cancers-11-01802" ref-type="bibr">194</xref>]. In order to elucidate the mechanism and improve personalized clinical treatment, systematical analysis of these common and specific lncRNAs is significant.</p><p>HOTAIR acts as a vital cancer-promoting lncRNA in the BC process, and it was found to be up-regulated in the three described subtypes (ER-positive, HER2-positive and TNBC) of the disease [<xref rid="B195-cancers-11-01802" ref-type="bibr">195</xref>,<xref rid="B196-cancers-11-01802" ref-type="bibr">196</xref>]. After assessing the expression profile of BC subtypes, Mathias et al. found down-regulation of LINC0051 in the ER-positive subtypes and upregulation in HER2-positive and TNBC subtypes. Additionally, MEG3, LINC00152, DANCR, and MALAT1 were linked to ER-positive and TNBC subtypes. When it comes to TNBC and HER2-positive subtypes, only GAS5 was commonly expressed [<xref rid="B195-cancers-11-01802" ref-type="bibr">195</xref>]. By conducting RNAseq of seven pairs of HER2-positive tumor vs non-tumor tissues, Yang et al. demonstrated that LOC100288637 is the highest positive correlative lncRNA with HER2, while RPL13P5 is the highest negative correlative one [<xref rid="B197-cancers-11-01802" ref-type="bibr">197</xref>].</p><p>As is commonly known, the description of basal-like BC usually regards cell aggressiveness, stem-like phenotype, poor prognosis, and high rates of metastasis [<xref rid="B198-cancers-11-01802" ref-type="bibr">198</xref>]. In the basal-like subtype-related network, three significantly dysregulated lncRNAs, including NEAT1, FAM83H-AS1 and XIST, were further investigated. Liu et al. demonstrated that combined use of docetaxel and carboplatin in ovarian cancer could rescue the down-regulated XIST expression [<xref rid="B199-cancers-11-01802" ref-type="bibr">199</xref>]. Thus, we consider that XIST may be a proper example to explain drug repositioning.</p><p>One possible mechanism that links the regulation on lncRNAs to some specific subtype may be associated with specific hormone receptors. In BC cells, under hormone stimulation or deprivation, estrogen could regulate lncRNAs expression via estrogen binding or independent of estrogen binding mechanism (Apo-ER) [<xref rid="B200-cancers-11-01802" ref-type="bibr">200</xref>]. The regulation on SNHG3, TINCR, HOTAIR, LINC00067, etc. expression is ligand dependent; the regulation on DANCR, LINC01016, DSCAM-AS1, etc. expression is ligand independent [<xref rid="B195-cancers-11-01802" ref-type="bibr">195</xref>]. Among them, HOTAIR’s expression is induced after 17β-estradiol (E2) treatment in BC cells, indicating that HOTAIR’ expression may be associated with estrogen receptors [<xref rid="B196-cancers-11-01802" ref-type="bibr">196</xref>]. Achievements in clinical treatment strategies have improved the survival and prognosis of BC patients. Based on the mechanisms of how lncRNAs promote tumor invasion and metastasis, researchers have begun to use drugs to regulate the expression of lncRNAs in order to impede tumor metastasis. Zhao et al. showed that a high concentration of 17b-estriol could impair the promotion of MALAT1 in the growth, invasion, and metastasis of BC cell lines by reducing lncRNA MALAT-1 expression in a dose-dependent manner [<xref rid="B201-cancers-11-01802" ref-type="bibr">201</xref>]. In addition, the presence of acquired and de-novo resistance is still a serious concern. Many researchers have illustrated crosstalk between resistance and metastasis, which relies on EMT, plasticity acquisition, tumor heterogeneity, and so forth [<xref rid="B202-cancers-11-01802" ref-type="bibr">202</xref>,<xref rid="B203-cancers-11-01802" ref-type="bibr">203</xref>,<xref rid="B204-cancers-11-01802" ref-type="bibr">204</xref>,<xref rid="B205-cancers-11-01802" ref-type="bibr">205</xref>]. At present, research uncovering whether and how lncRNAs function during the treatment of BC is relatively sufficient, and some of them, as we discussed above, have helped to gain a better understanding of the molecular mechanisms in chemotherapy resistance. In terms of radiotherapy, the relationship between lncRNAs and radiosensitization was first demonstrated in nasopharyngeal carcinoma cells. Huang et al. showed that the lncRNA Cur enhanced radiosensitization in nasopharyngeal carcinoma cells [<xref rid="B206-cancers-11-01802" ref-type="bibr">206</xref>]. To the best of our knowledge, in BC, HOTAIR and LINP1 were the initially investigated lncRNAs that may regulate BC radiosensitization. Knockdown of HOTAIR sensitizes BC cells to ionizing radiation through activating miR-218 [<xref rid="B207-cancers-11-01802" ref-type="bibr">207</xref>]. Overexpression of LINP1 enhances the survival of BC cells exposed to radiation [<xref rid="B208-cancers-11-01802" ref-type="bibr">208</xref>].</p><p>An understanding of the networks between lncRNAs, target miRNAs and genes, and BC metastasis is very useful. Besides the expression profile of lncRNAs, more functional and mechanistic investigations of lncRNA regulation of BCSC, cell autophagy and anoikis are required. Happily, lncRNAs have been in the center of public discussion since 5 years ago. This review helps to systematically understandi the molecular underpinning for finding more clinical biomarkers and treatment targets for BC in the near future.</p></sec></body><back><ack><title>Acknowledgments</title><p>We would like to thank the technical support by Xing-Hua Xiao, and the support from our families and friends.</p></ack><notes><title>Author Contributions</title><p>All authors contributed to the study conception and design. Material preparation was performed by Q.-Y.H. (Qi-Yuan Huang) and G.-F.L. Data collection and analysis were performed by Q.-Y.H. (Qi-Yuan Huang), G.-F.L., X.-L.Q., and L.-B.T. The first draft of the manuscript was written by Q.-Y.H. (Qi-Yuan Huang), L.-B.T., and Q.-Y.H. (Qing-Yun Huang). X.-L.Q. and L.-X.X. critically revised the work. All authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.</p></notes><notes><title>Funding</title><p>This research was funded by the National Natural Science Foundation of China (nos. 31860317).</p></notes><notes notes-type="COI-statement"><title>Conflicts of Interest</title><p>The authors declare no conflict of interest.</p></notes><ref-list><title>References</title><ref id="B1-cancers-11-01802"><label>1.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bray</surname><given-names>F.</given-names></name><name><surname>Ferlay</surname><given-names>J.</given-names></name><name><surname>Soerjomataram</surname><given-names>I.</given-names></name><name><surname>Siegel</surname><given-names>R.</given-names></name><name><surname>Torre</surname><given-names>L.</given-names></name><name><surname>Jemal</surname><given-names>A.</given-names></name></person-group><article-title>Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries</article-title><source>CA Cancer J. Clin.</source><year>2018</year><volume>68</volume><fpage>394</fpage><lpage>424</lpage><pub-id pub-id-type="doi">10.3322/caac.21492</pub-id><pub-id pub-id-type="pmid">30207593</pub-id></element-citation></ref><ref id="B2-cancers-11-01802"><label>2.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pondé</surname><given-names>N.</given-names></name><name><surname>Brandão</surname><given-names>M.</given-names></name><name><surname>El-Hachem</surname><given-names>G.</given-names></name><name><surname>Werbrouck</surname><given-names>E.</given-names></name><name><surname>Piccart</surname><given-names>M.</given-names></name></person-group><article-title>Treatment of advanced HER2-positive breast cancer: 2018 and beyond</article-title><source>Cancer Treat. Rev.</source><year>2018</year><volume>67</volume><fpage>10</fpage><lpage>20</lpage><pub-id pub-id-type="doi">10.1016/j.ctrv.2018.04.016</pub-id><pub-id pub-id-type="pmid">29751334</pub-id></element-citation></ref><ref id="B3-cancers-11-01802"><label>3.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Suba</surname><given-names>Z.</given-names></name></person-group><article-title>Triple-negative breast cancer risk in women is defined by the defect of estrogen signaling: Preventive and therapeutic implications</article-title><source>Onco Targets Ther.</source><year>2014</year><volume>7</volume><fpage>147</fpage><lpage>164</lpage><pub-id pub-id-type="doi">10.2147/OTT.S52600</pub-id><pub-id pub-id-type="pmid">24482576</pub-id></element-citation></ref><ref id="B4-cancers-11-01802"><label>4.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gadi</surname><given-names>V.K.</given-names></name><name><surname>Davidson</surname><given-names>N.E.</given-names></name></person-group><article-title>Practical Approach to Triple-Negative Breast Cancer</article-title><source>J. Oncol. Pract.</source><year>2017</year><volume>13</volume><fpage>293</fpage><lpage>300</lpage><pub-id pub-id-type="doi">10.1200/JOP.2017.022632</pub-id><pub-id pub-id-type="pmid">28489980</pub-id></element-citation></ref><ref id="B5-cancers-11-01802"><label>5.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Rabanal</surname><given-names>C.</given-names></name><name><surname>Ruiz</surname><given-names>R.</given-names></name><name><surname>Neciosup</surname><given-names>S.</given-names></name><name><surname>Gomez</surname><given-names>H.</given-names></name></person-group><article-title>Metronomic chemotherapy for non-metastatic triple negative breast cancer: Selection is the key</article-title><source>World J. Clin. Oncol.</source><year>2017</year><volume>8</volume><fpage>437</fpage><lpage>446</lpage><pub-id pub-id-type="doi">10.5306/wjco.v8.i6.437</pub-id><pub-id pub-id-type="pmid">29291168</pub-id></element-citation></ref><ref id="B6-cancers-11-01802"><label>6.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pastushenko</surname><given-names>I.</given-names></name><name><surname>Brisebarre</surname><given-names>A.</given-names></name><name><surname>Sifrim</surname><given-names>A.</given-names></name><name><surname>Fioramonti</surname><given-names>M.</given-names></name><name><surname>Revenco</surname><given-names>T.</given-names></name><name><surname>Boumahdi</surname><given-names>S.</given-names></name><name><surname>Van Keymeulen</surname><given-names>A.</given-names></name><name><surname>Brown</surname><given-names>D.</given-names></name><name><surname>Moers</surname><given-names>V.</given-names></name><name><surname>Lemaire</surname><given-names>S.</given-names></name><etal></etal></person-group><article-title>Identification of the tumour transition states occurring during EMT</article-title><source>Nature</source><year>2018</year><volume>556</volume><fpage>463</fpage><lpage>468</lpage><pub-id pub-id-type="doi">10.1038/s41586-018-0040-3</pub-id><pub-id pub-id-type="pmid">29670281</pub-id></element-citation></ref><ref id="B7-cancers-11-01802"><label>7.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mitra</surname><given-names>A.</given-names></name><name><surname>Mishra</surname><given-names>L.</given-names></name><name><surname>Li</surname><given-names>S.</given-names></name></person-group><article-title>EMT, CTCs and CSCs in tumor relapse and drug-resistance</article-title><source>Oncotarget</source><year>2015</year><volume>6</volume><fpage>10697</fpage><lpage>10711</lpage><pub-id pub-id-type="doi">10.18632/oncotarget.4037</pub-id><pub-id pub-id-type="pmid">25986923</pub-id></element-citation></ref><ref id="B8-cancers-11-01802"><label>8.</label><element-citation publication-type="journal"><person-group person-group-type="author"><collab>The ENCODE Project Consortium</collab></person-group><article-title>An integrated encyclopedia of DNA elements in the human genome</article-title><source>Nature</source><year>2012</year><volume>489</volume><fpage>57</fpage><lpage>74</lpage><pub-id pub-id-type="doi">10.1038/nature11247</pub-id><pub-id pub-id-type="pmid">22955616</pub-id></element-citation></ref><ref id="B9-cancers-11-01802"><label>9.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Morris</surname><given-names>K.V.</given-names></name><name><surname>Mattick</surname><given-names>J.S.</given-names></name></person-group><article-title>The rise of regulatory RNA</article-title><source>Nat. Rev. Genet.</source><year>2014</year><volume>15</volume><fpage>423</fpage><lpage>437</lpage><pub-id pub-id-type="doi">10.1038/nrg3722</pub-id><pub-id pub-id-type="pmid">24776770</pub-id></element-citation></ref><ref id="B10-cancers-11-01802"><label>10.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ponting</surname><given-names>C.P.</given-names></name><name><surname>Oliver</surname><given-names>P.L.</given-names></name><name><surname>Reik</surname><given-names>W.</given-names></name></person-group><article-title>Evolution and functions of long noncoding RNAs</article-title><source>Cell</source><year>2009</year><volume>136</volume><fpage>629</fpage><lpage>641</lpage><pub-id pub-id-type="doi">10.1016/j.cell.2009.02.006</pub-id><pub-id pub-id-type="pmid">19239885</pub-id></element-citation></ref><ref id="B11-cancers-11-01802"><label>11.</label><element-citation publication-type="web"><article-title>GENECODE</article-title><comment>Available online: <ext-link ext-link-type="uri" xlink:href="https://www.gencodegenes.org/">https://www.gencodegenes.org/</ext-link></comment><date-in-citation content-type="access-date" iso-8601-date="2019-09-19">(accessed on 19 September 2019)</date-in-citation></element-citation></ref><ref id="B12-cancers-11-01802"><label>12.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Evans</surname><given-names>J.R.</given-names></name><name><surname>Feng</surname><given-names>F.Y.</given-names></name><name><surname>Chinnaiyan</surname><given-names>A.M.</given-names></name></person-group><article-title>The bright side of dark matter: lncRNAs in cancer</article-title><source>J. Clin. Investig.</source><year>2016</year><volume>126</volume><fpage>2775</fpage><pub-id pub-id-type="doi">10.1172/JCI84421</pub-id><pub-id pub-id-type="pmid">27479746</pub-id></element-citation></ref><ref id="B13-cancers-11-01802"><label>13.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Congrains</surname><given-names>A.</given-names></name><name><surname>Kamide</surname><given-names>K.</given-names></name><name><surname>Oguro</surname><given-names>R.</given-names></name><name><surname>Yasuda</surname><given-names>O.</given-names></name><name><surname>Miyata</surname><given-names>K.</given-names></name><name><surname>Yamamoto</surname><given-names>E.</given-names></name><name><surname>Kawai</surname><given-names>T.</given-names></name><name><surname>Kusunoki</surname><given-names>H.</given-names></name><name><surname>Yamamoto</surname><given-names>H.</given-names></name><name><surname>Takeya</surname><given-names>Y.</given-names></name><etal></etal></person-group><article-title>Genetic variants at the 9p21 locus contribute to atherosclerosis through modulation of ANRIL and CDKN2A/B</article-title><source>Atherosclerosis</source><year>2012</year><volume>220</volume><fpage>449</fpage><lpage>455</lpage><pub-id pub-id-type="doi">10.1016/j.atherosclerosis.2011.11.017</pub-id><pub-id pub-id-type="pmid">22178423</pub-id></element-citation></ref><ref id="B14-cancers-11-01802"><label>14.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>Y.</given-names></name><name><surname>Cai</surname><given-names>Y.</given-names></name><name><surname>Wu</surname><given-names>G.</given-names></name><name><surname>Chen</surname><given-names>X.</given-names></name><name><surname>Liu</surname><given-names>Y.</given-names></name><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Yu</surname><given-names>J.</given-names></name><name><surname>Li</surname><given-names>C.</given-names></name><name><surname>Chen</surname><given-names>X.</given-names></name><name><surname>Jose</surname><given-names>P.</given-names></name><etal></etal></person-group><article-title>Plasma long non-coding RNA, CoroMarker, a novel biomarker for diagnosis of coronary artery disease</article-title><source>Clin. Sci.</source><year>2015</year><volume>129</volume><fpage>675</fpage><lpage>685</lpage><pub-id pub-id-type="doi">10.1042/CS20150121</pub-id><pub-id pub-id-type="pmid">26201019</pub-id></element-citation></ref><ref id="B15-cancers-11-01802"><label>15.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ashraf</surname><given-names>G.</given-names></name><name><surname>Ganash</surname><given-names>M.</given-names></name><name><surname>Athanasios</surname><given-names>A.</given-names></name></person-group><article-title>Computational analysis of non-coding RNAs in Alzheimer‘s disease</article-title><source>Bioinformation</source><year>2019</year><volume>15</volume><fpage>351</fpage><lpage>357</lpage><pub-id pub-id-type="doi">10.6026/97320630015351</pub-id><pub-id pub-id-type="pmid">31249438</pub-id></element-citation></ref><ref id="B16-cancers-11-01802"><label>16.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Huang</surname><given-names>X.</given-names></name><name><surname>Luo</surname><given-names>Y.L.</given-names></name><name><surname>Mao</surname><given-names>Y.S.</given-names></name><name><surname>Ji</surname><given-names>J.L.</given-names></name></person-group><article-title>The link between long noncoding RNAs and depression</article-title><source>Prog. Neuropsychopharmacol. Biol. Psychiatry</source><year>2017</year><volume>73</volume><fpage>73</fpage><lpage>78</lpage><pub-id pub-id-type="doi">10.1016/j.pnpbp.2016.06.004</pub-id><pub-id pub-id-type="pmid">27318257</pub-id></element-citation></ref><ref id="B17-cancers-11-01802"><label>17.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mirza</surname><given-names>A.H.</given-names></name><name><surname>Kaur</surname><given-names>S.</given-names></name><name><surname>Pociot</surname><given-names>F.</given-names></name></person-group><article-title>Long non-coding RNAs as novel players in β cell function and type 1 diabetes</article-title><source>Hum. Genom.</source><year>2017</year><volume>11</volume><fpage>17</fpage><pub-id pub-id-type="doi">10.1186/s40246-017-0113-7</pub-id></element-citation></ref><ref id="B18-cancers-11-01802"><label>18.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lorenzi</surname><given-names>L.</given-names></name><name><surname>Avila Cobos</surname><given-names>F.</given-names></name><name><surname>Decock</surname><given-names>A.</given-names></name><name><surname>Everaert</surname><given-names>C.</given-names></name><name><surname>Helsmoortel</surname><given-names>H.</given-names></name><name><surname>Lefever</surname><given-names>S.</given-names></name><name><surname>Verboom</surname><given-names>K.</given-names></name><name><surname>Volders</surname><given-names>P.</given-names></name><name><surname>Speleman</surname><given-names>F.</given-names></name><name><surname>Vandesompele</surname><given-names>J.</given-names></name><etal></etal></person-group><article-title>Long noncoding RNA expression profiling in cancer: Challenges and opportunities</article-title><source>GenesChromosomes Cancer</source><year>2019</year><volume>58</volume><fpage>191</fpage><lpage>199</lpage><pub-id pub-id-type="doi">10.1002/gcc.22709</pub-id></element-citation></ref><ref id="B19-cancers-11-01802"><label>19.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Angrand</surname><given-names>P.</given-names></name><name><surname>Vennin</surname><given-names>C.</given-names></name><name><surname>Le Bourhis</surname><given-names>X.</given-names></name><name><surname>Adriaenssens</surname><given-names>E.</given-names></name></person-group><article-title>The role of long non-coding RNAs in genome formatting and expression</article-title><source>Front. Genet.</source><year>2015</year><volume>6</volume><fpage>165</fpage><pub-id pub-id-type="doi">10.3389/fgene.2015.00165</pub-id><pub-id pub-id-type="pmid">25972893</pub-id></element-citation></ref><ref id="B20-cancers-11-01802"><label>20.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Fan</surname><given-names>C.</given-names></name><name><surname>Ma</surname><given-names>L.</given-names></name><name><surname>Liu</surname><given-names>N.</given-names></name></person-group><article-title>Systematic analysis of lncRNA-miRNA-mRNA competing endogenous RNA network identifies four-lncRNA signature as a prognostic biomarker for breast cancer</article-title><source>J. Transl. Med.</source><year>2018</year><volume>16</volume><fpage>264</fpage><pub-id pub-id-type="doi">10.1186/s12967-018-1640-2</pub-id><pub-id pub-id-type="pmid">30261893</pub-id></element-citation></ref><ref id="B21-cancers-11-01802"><label>21.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Huang</surname><given-names>Y.</given-names></name></person-group><article-title>The novel regulatory role of lncRNA-miRNA-mRNA axis in cardiovascular diseases</article-title><source>J. Cell. Mol. Med.</source><year>2018</year><volume>22</volume><fpage>5768</fpage><lpage>5775</lpage><pub-id pub-id-type="doi">10.1111/jcmm.13866</pub-id><pub-id pub-id-type="pmid">30188595</pub-id></element-citation></ref><ref id="B22-cancers-11-01802"><label>22.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lian</surname><given-names>Y.</given-names></name><name><surname>Xiong</surname><given-names>F.</given-names></name><name><surname>Yang</surname><given-names>L.</given-names></name><name><surname>Bo</surname><given-names>H.</given-names></name><name><surname>Gong</surname><given-names>Z.</given-names></name><name><surname>Wang</surname><given-names>Y.</given-names></name><name><surname>Wei</surname><given-names>F.</given-names></name><name><surname>Tang</surname><given-names>Y.</given-names></name><name><surname>Li</surname><given-names>X.</given-names></name><name><surname>Liao</surname><given-names>Q.</given-names></name><etal></etal></person-group><article-title>Long noncoding RNA AFAP1-AS1 acts as a competing endogenous RNA of miR-423-5p to facilitate nasopharyngeal carcinoma metastasis through regulating the Rho/Rac pathway</article-title><source>J. Exp. Clin. Cancer Res. CR</source><year>2018</year><volume>37</volume><fpage>253</fpage><pub-id pub-id-type="doi">10.1186/s13046-018-0918-9</pub-id><pub-id pub-id-type="pmid">30326930</pub-id></element-citation></ref><ref id="B23-cancers-11-01802"><label>23.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>X.</given-names></name><name><surname>Cheng</surname><given-names>T.</given-names></name><name><surname>He</surname><given-names>Q.</given-names></name><name><surname>Lei</surname><given-names>Z.</given-names></name><name><surname>Chi</surname><given-names>J.</given-names></name><name><surname>Tang</surname><given-names>Z.</given-names></name><name><surname>Liao</surname><given-names>Q.</given-names></name><name><surname>Zhang</surname><given-names>H.</given-names></name><name><surname>Zeng</surname><given-names>L.</given-names></name><name><surname>Cui</surname><given-names>S.</given-names></name></person-group><article-title>LINC01133 as ceRNA inhibits gastric cancer progression by sponging miR-106a-3p to regulate APC expression and the Wnt/β-catenin pathway</article-title><source>Mol. Cancer</source><year>2018</year><volume>17</volume><fpage>126</fpage><pub-id pub-id-type="doi">10.1186/s12943-018-0874-1</pub-id><pub-id pub-id-type="pmid">30134915</pub-id></element-citation></ref><ref id="B24-cancers-11-01802"><label>24.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Leucci</surname><given-names>E.</given-names></name></person-group><article-title>Cancer development and therapy resistance: Spotlights on the dark side of the genome</article-title><source>Pharmacol. Ther.</source><year>2018</year><volume>189</volume><fpage>22</fpage><lpage>30</lpage><pub-id pub-id-type="doi">10.1016/j.pharmthera.2018.04.001</pub-id><pub-id pub-id-type="pmid">29649500</pub-id></element-citation></ref><ref id="B25-cancers-11-01802"><label>25.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yuan</surname><given-names>S.</given-names></name><name><surname>Wang</surname><given-names>J.</given-names></name><name><surname>Yang</surname><given-names>F.</given-names></name><name><surname>Tao</surname><given-names>Q.</given-names></name><name><surname>Zhang</surname><given-names>J.</given-names></name><name><surname>Wang</surname><given-names>L.</given-names></name><name><surname>Yang</surname><given-names>Y.</given-names></name><name><surname>Liu</surname><given-names>H.</given-names></name><name><surname>Wang</surname><given-names>Z.</given-names></name><name><surname>Xu</surname><given-names>Q.</given-names></name><etal></etal></person-group><article-title>Long noncoding RNA DANCR increases stemness features of hepatocellular carcinoma by derepression of CTNNB1</article-title><source>Hepatology</source><year>2016</year><volume>63</volume><fpage>499</fpage><lpage>511</lpage><pub-id pub-id-type="doi">10.1002/hep.27893</pub-id><pub-id pub-id-type="pmid">25964079</pub-id></element-citation></ref><ref id="B26-cancers-11-01802"><label>26.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>Y.</given-names></name><name><surname>Zhang</surname><given-names>M.</given-names></name><name><surname>Liang</surname><given-names>L.</given-names></name><name><surname>Li</surname><given-names>J.</given-names></name><name><surname>Chen</surname><given-names>Y.</given-names></name></person-group><article-title>Over-expression of lncRNA DANCR is associated with advanced tumor progression and poor prognosis in patients with colorectal cancer</article-title><source>Int. J. Clin. Exp. Pathol.</source><year>2015</year><volume>8</volume><fpage>11480</fpage><lpage>11484</lpage><pub-id pub-id-type="pmid">26617879</pub-id></element-citation></ref><ref id="B27-cancers-11-01802"><label>27.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sha</surname><given-names>S.</given-names></name><name><surname>Yuan</surname><given-names>D.</given-names></name><name><surname>Liu</surname><given-names>Y.</given-names></name><name><surname>Han</surname><given-names>B.</given-names></name><name><surname>Zhong</surname><given-names>N.</given-names></name></person-group><article-title>Targeting long non-coding RNA DANCR inhibits triple negative breast cancer progression</article-title><source>Biol. Open</source><year>2017</year><volume>6</volume><fpage>1310</fpage><lpage>1316</lpage><pub-id pub-id-type="doi">10.1242/bio.023135</pub-id><pub-id pub-id-type="pmid">28760736</pub-id></element-citation></ref><ref id="B28-cancers-11-01802"><label>28.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hock</surname><given-names>H.</given-names></name></person-group><article-title>A complex Polycomb issue: The two faces of EZH2 in cancer</article-title><source>Genes Dev.</source><year>2012</year><volume>26</volume><fpage>751</fpage><lpage>755</lpage><pub-id pub-id-type="doi">10.1101/gad.191163.112</pub-id><pub-id pub-id-type="pmid">22508723</pub-id></element-citation></ref><ref id="B29-cancers-11-01802"><label>29.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Vaidya</surname><given-names>A.M.</given-names></name><name><surname>Sun</surname><given-names>Z.</given-names></name><name><surname>Ayat</surname><given-names>N.</given-names></name><name><surname>Schilb</surname><given-names>A.</given-names></name><name><surname>Liu</surname><given-names>X.</given-names></name><name><surname>Jiang</surname><given-names>H.</given-names></name><name><surname>Sun</surname><given-names>D.</given-names></name><name><surname>Scheidt</surname><given-names>J.</given-names></name><name><surname>Qian</surname><given-names>V.</given-names></name><name><surname>He</surname><given-names>S.</given-names></name><etal></etal></person-group><article-title>Systemic Delivery of Tumor-Targeting siRNA Nanoparticles against an Oncogenic LncRNA Facilitates Effective Triple-Negative Breast Cancer Therapy</article-title><source>Bioconj. Chem.</source><year>2019</year><pub-id pub-id-type="doi">10.1021/acs.bioconjchem.9b00028</pub-id></element-citation></ref><ref id="B30-cancers-11-01802"><label>30.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tao</surname><given-names>W.</given-names></name><name><surname>Wang</surname><given-names>C.</given-names></name><name><surname>Zhu</surname><given-names>B.</given-names></name><name><surname>Zhang</surname><given-names>G.</given-names></name><name><surname>Pang</surname><given-names>D.</given-names></name></person-group><article-title>LncRNA DANCR contributes to tumor progression via targetting miR-216a-5p in breast cancer: lncRNA DANCR contributes to tumor progression</article-title><source>Biosci. Rep.</source><year>2019</year><volume>39</volume><pub-id pub-id-type="doi">10.1042/BSR20181618</pub-id></element-citation></ref><ref id="B31-cancers-11-01802"><label>31.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Muller</surname><given-names>V.</given-names></name><name><surname>Ferrer</surname><given-names>L.O.</given-names></name><name><surname>Steinbach</surname><given-names>B.</given-names></name><name><surname>Pantel</surname><given-names>K.</given-names></name><name><surname>Schwarzenbach</surname><given-names>H.</given-names></name></person-group><article-title>Interplay of lncRNA H19/miR-675 and lncRNA NEAT1/miR-204 in breast cancer</article-title><source>Mol. Oncol.</source><year>2019</year><pub-id pub-id-type="doi">10.1002/1878-0261.12472</pub-id></element-citation></ref><ref id="B32-cancers-11-01802"><label>32.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lottin</surname><given-names>S.</given-names></name><name><surname>Adriaenssens</surname><given-names>E.</given-names></name><name><surname>Dupressoir</surname><given-names>T.</given-names></name><name><surname>Berteaux</surname><given-names>N.</given-names></name><name><surname>Montpellier</surname><given-names>C.</given-names></name><name><surname>Coll</surname><given-names>J.</given-names></name><name><surname>Dugimont</surname><given-names>T.</given-names></name><name><surname>Curgy</surname><given-names>J.J.</given-names></name></person-group><article-title>Overexpression of an ectopic H19 gene enhances the tumorigenic properties of breast cancer cells</article-title><source>Carcinogenesis</source><year>2002</year><volume>23</volume><fpage>1885</fpage><lpage>1895</lpage><pub-id pub-id-type="doi">10.1093/carcin/23.11.1885</pub-id><pub-id pub-id-type="pmid">12419837</pub-id></element-citation></ref><ref id="B33-cancers-11-01802"><label>33.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kastl</surname><given-names>L.</given-names></name><name><surname>Brown</surname><given-names>I.</given-names></name><name><surname>Schofield</surname><given-names>A.C.</given-names></name></person-group><article-title>Altered DNA methylation is associated with docetaxel resistance in human breast cancer cells</article-title><source>Int. J. Oncol.</source><year>2010</year><volume>36</volume><fpage>1235</fpage><lpage>1241</lpage><pub-id pub-id-type="pmid">20372798</pub-id></element-citation></ref><ref id="B34-cancers-11-01802"><label>34.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Rajabi</surname><given-names>H.</given-names></name><name><surname>Tagde</surname><given-names>A.</given-names></name><name><surname>Alam</surname><given-names>M.</given-names></name><name><surname>Bouillez</surname><given-names>A.</given-names></name><name><surname>Pitroda</surname><given-names>S.</given-names></name><name><surname>Suzuki</surname><given-names>Y.</given-names></name><name><surname>Kufe</surname><given-names>D.</given-names></name></person-group><article-title>DNA methylation by DNMT1 and DNMT3b methyltransferases is driven by the MUC1-C oncoprotein in human carcinoma cells</article-title><source>Oncogene</source><year>2016</year><volume>35</volume><fpage>6439</fpage><lpage>6445</lpage><pub-id pub-id-type="doi">10.1038/onc.2016.180</pub-id><pub-id pub-id-type="pmid">27212035</pub-id></element-citation></ref><ref id="B35-cancers-11-01802"><label>35.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>W.</given-names></name><name><surname>Chang</surname><given-names>Z.</given-names></name><name><surname>Shi</surname><given-names>K.E.</given-names></name><name><surname>Song</surname><given-names>L.</given-names></name><name><surname>Cui</surname><given-names>L.I.</given-names></name><name><surname>Ma</surname><given-names>Z.</given-names></name><name><surname>Li</surname><given-names>X.</given-names></name><name><surname>Ma</surname><given-names>W.</given-names></name><name><surname>Wang</surname><given-names>L.</given-names></name></person-group><article-title>The correlation between DNMT1 and ERalpha expression and the methylation status of ERalpha, and its clinical significance in breast cancer</article-title><source>Oncol. Lett.</source><year>2016</year><volume>11</volume><fpage>1995</fpage><lpage>2000</lpage><pub-id pub-id-type="doi">10.3892/ol.2016.4193</pub-id><pub-id pub-id-type="pmid">26998112</pub-id></element-citation></ref><ref id="B36-cancers-11-01802"><label>36.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>Z.</given-names></name><name><surname>Li</surname><given-names>Y.</given-names></name><name><surname>Li</surname><given-names>Y.</given-names></name><name><surname>Ren</surname><given-names>K.</given-names></name><name><surname>Li</surname><given-names>X.</given-names></name><name><surname>Han</surname><given-names>X.</given-names></name><name><surname>Wang</surname><given-names>J.</given-names></name></person-group><article-title>Long non-coding RNA H19 promotes the proliferation and invasion of breast cancer through upregulating DNMT1 expression by sponging miR-152</article-title><source>J. Biochem. Mol. Toxicol.</source><year>2017</year><volume>31</volume><pub-id pub-id-type="doi">10.1002/jbt.21933</pub-id></element-citation></ref><ref id="B37-cancers-11-01802"><label>37.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bates</surname><given-names>P.</given-names></name><name><surname>Fisher</surname><given-names>R.</given-names></name><name><surname>Ward</surname><given-names>A.</given-names></name><name><surname>Richardson</surname><given-names>L.</given-names></name><name><surname>Hill</surname><given-names>D.J.</given-names></name><name><surname>Graham</surname><given-names>C.F.</given-names></name></person-group><article-title>Mammary cancer in transgenic mice expressing insulin-like growth factor II (IGF-II)</article-title><source>Br. J. Cancer</source><year>1995</year><volume>72</volume><fpage>1189</fpage><lpage>1193</lpage><pub-id pub-id-type="doi">10.1038/bjc.1995.484</pub-id><pub-id pub-id-type="pmid">7577466</pub-id></element-citation></ref><ref id="B38-cancers-11-01802"><label>38.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Min</surname><given-names>H.</given-names></name><name><surname>Lee</surname><given-names>S.</given-names></name><name><surname>Woo</surname><given-names>J.</given-names></name><name><surname>Jung</surname><given-names>H.</given-names></name><name><surname>Park</surname><given-names>K.</given-names></name><name><surname>Jeong</surname><given-names>H.</given-names></name><name><surname>Hyun</surname><given-names>S.</given-names></name><name><surname>Cho</surname><given-names>J.</given-names></name><name><surname>Lee</surname><given-names>W.</given-names></name><name><surname>Park</surname><given-names>J.</given-names></name><etal></etal></person-group><article-title>Essential role of DNA methyltransferase 1-mediated transcription of insulin-like growth factor 2 in resistance to histone deacetylase inhibitors</article-title><source>Clin. Cancer Res.</source><year>2017</year><volume>23</volume><fpage>1299</fpage><lpage>1311</lpage><pub-id pub-id-type="doi">10.1158/1078-0432.CCR-16-0534</pub-id><pub-id pub-id-type="pmid">27582487</pub-id></element-citation></ref><ref id="B39-cancers-11-01802"><label>39.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Vennin</surname><given-names>C.</given-names></name><name><surname>Spruyt</surname><given-names>N.</given-names></name><name><surname>Robin</surname><given-names>Y.M.</given-names></name><name><surname>Chassat</surname><given-names>T.</given-names></name><name><surname>Le Bourhis</surname><given-names>X.</given-names></name><name><surname>Adriaenssens</surname><given-names>E.</given-names></name></person-group><article-title>The long non-coding RNA 91H increases aggressive phenotype of breast cancer cells and up-regulates H19/IGF2 expression through epigenetic modifications</article-title><source>Cancer Lett.</source><year>2017</year><volume>385</volume><fpage>198</fpage><lpage>206</lpage><pub-id pub-id-type="doi">10.1016/j.canlet.2016.10.023</pub-id><pub-id pub-id-type="pmid">27780718</pub-id></element-citation></ref><ref id="B40-cancers-11-01802"><label>40.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tran</surname><given-names>V.</given-names></name><name><surname>Court</surname><given-names>F.</given-names></name><name><surname>Duputié</surname><given-names>A.</given-names></name><name><surname>Antoine</surname><given-names>E.</given-names></name><name><surname>Aptel</surname><given-names>N.</given-names></name><name><surname>Milligan</surname><given-names>L.</given-names></name><name><surname>Carbonell</surname><given-names>F.</given-names></name><name><surname>Lelay-Taha</surname><given-names>M.</given-names></name><name><surname>Piette</surname><given-names>J.</given-names></name><name><surname>Weber</surname><given-names>M.</given-names></name><etal></etal></person-group><article-title>H19 antisense RNA can up-regulate Igf2 transcription by activation of a novel promoter in mouse myoblasts</article-title><source>PLoS ONE</source><year>2012</year><volume>7</volume><elocation-id>e37923</elocation-id><pub-id pub-id-type="doi">10.1371/journal.pone.0037923</pub-id><pub-id pub-id-type="pmid">22662250</pub-id></element-citation></ref><ref id="B41-cancers-11-01802"><label>41.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sørensen</surname><given-names>K.</given-names></name><name><surname>Thomassen</surname><given-names>M.</given-names></name><name><surname>Tan</surname><given-names>Q.</given-names></name><name><surname>Bak</surname><given-names>M.</given-names></name><name><surname>Cold</surname><given-names>S.</given-names></name><name><surname>Burton</surname><given-names>M.</given-names></name><name><surname>Larsen</surname><given-names>M.</given-names></name><name><surname>Kruse</surname><given-names>T.</given-names></name></person-group><article-title>Long non-coding RNA HOTAIR is an independent prognostic marker of metastasis in estrogen receptor-positive primary breast cancer</article-title><source>Breast Cancer Res. Treat.</source><year>2013</year><volume>142</volume><fpage>529</fpage><lpage>536</lpage><pub-id pub-id-type="doi">10.1007/s10549-013-2776-7</pub-id><pub-id pub-id-type="pmid">24258260</pub-id></element-citation></ref><ref id="B42-cancers-11-01802"><label>42.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhuang</surname><given-names>Y.</given-names></name><name><surname>Nguyen</surname><given-names>H.</given-names></name><name><surname>Burow</surname><given-names>M.</given-names></name><name><surname>Zhuo</surname><given-names>Y.</given-names></name><name><surname>El-Dahr</surname><given-names>S.</given-names></name><name><surname>Yao</surname><given-names>X.</given-names></name><name><surname>Cao</surname><given-names>S.</given-names></name><name><surname>Flemington</surname><given-names>E.</given-names></name><name><surname>Nephew</surname><given-names>K.</given-names></name><name><surname>Fang</surname><given-names>F.</given-names></name><etal></etal></person-group><article-title>Elevated expression of long intergenic non-coding RNA HOTAIR in a basal-like variant of MCF-7 breast cancer cells</article-title><source>Mol. Carcinog.</source><year>2015</year><volume>54</volume><fpage>1656</fpage><lpage>1667</lpage><pub-id pub-id-type="doi">10.1002/mc.22237</pub-id><pub-id pub-id-type="pmid">25328122</pub-id></element-citation></ref><ref id="B43-cancers-11-01802"><label>43.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kim</surname><given-names>H.J.</given-names></name><name><surname>Lee</surname><given-names>D.W.</given-names></name><name><surname>Yim</surname><given-names>G.W.</given-names></name><name><surname>Nam</surname><given-names>E.J.</given-names></name><name><surname>Kim</surname><given-names>S.</given-names></name><name><surname>Kim</surname><given-names>S.W.</given-names></name><name><surname>Kim</surname><given-names>Y.T.</given-names></name></person-group><article-title>Long non-coding RNA HOTAIR is associated with human cervical cancer progression</article-title><source>Int. J. Oncol.</source><year>2015</year><volume>46</volume><fpage>521</fpage><lpage>530</lpage><pub-id pub-id-type="doi">10.3892/ijo.2014.2758</pub-id><pub-id pub-id-type="pmid">25405331</pub-id></element-citation></ref><ref id="B44-cancers-11-01802"><label>44.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yu</surname><given-names>Y.</given-names></name><name><surname>Lv</surname><given-names>F.</given-names></name><name><surname>Liang</surname><given-names>D.</given-names></name><name><surname>Yang</surname><given-names>Q.</given-names></name><name><surname>Zhang</surname><given-names>B.</given-names></name><name><surname>Lin</surname><given-names>H.</given-names></name><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Qian</surname><given-names>G.</given-names></name><name><surname>Xu</surname><given-names>J.</given-names></name><name><surname>You</surname><given-names>W.</given-names></name></person-group><article-title>HOTAIR may regulate proliferation, apoptosis, migration and invasion of MCF-7 cells through regulating the P53/Akt/JNK signaling pathway</article-title><source>Biomed. Pharm.</source><year>2017</year><volume>90</volume><fpage>555</fpage><lpage>561</lpage><pub-id pub-id-type="doi">10.1016/j.biopha.2017.03.054</pub-id><pub-id pub-id-type="pmid">28407576</pub-id></element-citation></ref><ref id="B45-cancers-11-01802"><label>45.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Huang</surname><given-names>Y.</given-names></name><name><surname>Du</surname><given-names>J.</given-names></name><name><surname>Mi</surname><given-names>Y.</given-names></name><name><surname>Li</surname><given-names>T.</given-names></name><name><surname>Gong</surname><given-names>Y.</given-names></name><name><surname>Ouyang</surname><given-names>H.</given-names></name><name><surname>Hou</surname><given-names>Y.</given-names></name></person-group><article-title>Long Non-coding RNAs Contribute to the Inhibition of Proliferation and EMT by Pterostilbene in Human Breast Cancer</article-title><source>Front. Oncol.</source><year>2018</year><volume>8</volume><fpage>629</fpage><pub-id pub-id-type="doi">10.3389/fonc.2018.00629</pub-id><pub-id pub-id-type="pmid">30619763</pub-id></element-citation></ref><ref id="B46-cancers-11-01802"><label>46.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhao</surname><given-names>W.</given-names></name><name><surname>Geng</surname><given-names>D.</given-names></name><name><surname>Li</surname><given-names>S.</given-names></name><name><surname>Chen</surname><given-names>Z.</given-names></name><name><surname>Sun</surname><given-names>M.</given-names></name></person-group><article-title>LncRNA HOTAIR influences cell growth, migration, invasion, and apoptosis via the miR-20a-5p/HMGA2 axis in breast cancer</article-title><source>Cancer Med.</source><year>2018</year><volume>7</volume><fpage>842</fpage><lpage>855</lpage><pub-id pub-id-type="doi">10.1002/cam4.1353</pub-id><pub-id pub-id-type="pmid">29473328</pub-id></element-citation></ref><ref id="B47-cancers-11-01802"><label>47.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cogill</surname><given-names>S.B.</given-names></name><name><surname>Wang</surname><given-names>L.</given-names></name></person-group><article-title>Co-expression Network Analysis of Human lncRNAs and Cancer Genes</article-title><source>Cancer Inf.</source><year>2014</year><volume>13</volume><fpage>49</fpage><lpage>59</lpage><pub-id pub-id-type="doi">10.4137/CIN.S14070</pub-id></element-citation></ref><ref id="B48-cancers-11-01802"><label>48.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wu</surname><given-names>J.</given-names></name><name><surname>Shuang</surname><given-names>Z.</given-names></name><name><surname>Zhao</surname><given-names>J.</given-names></name><name><surname>Tang</surname><given-names>H.</given-names></name><name><surname>Liu</surname><given-names>P.</given-names></name><name><surname>Zhang</surname><given-names>L.</given-names></name><name><surname>Xie</surname><given-names>X.</given-names></name><name><surname>Xiao</surname><given-names>X.</given-names></name></person-group><article-title>Linc00152 promotes tumorigenesis by regulating DNMTs in triple-negative breast cancer</article-title><source>Biomed. Pharm.</source><year>2018</year><volume>97</volume><fpage>1275</fpage><lpage>1281</lpage><pub-id pub-id-type="doi">10.1016/j.biopha.2017.11.055</pub-id></element-citation></ref><ref id="B49-cancers-11-01802"><label>49.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hu</surname><given-names>X.L.</given-names></name><name><surname>Wang</surname><given-names>J.</given-names></name><name><surname>He</surname><given-names>W.</given-names></name><name><surname>Zhao</surname><given-names>P.</given-names></name><name><surname>Wu</surname><given-names>W.Q.</given-names></name></person-group><article-title>Down-regulation of lncRNA Linc00152 suppressed cell viability, invasion, migration, and epithelial to mesenchymal transition, and reversed chemo-resistance in breast cancer cells</article-title><source>Eur. Rev. Med. Pharmacol. Sci.</source><year>2018</year><volume>22</volume><fpage>3074</fpage><lpage>3084</lpage><pub-id pub-id-type="pmid">29863253</pub-id></element-citation></ref><ref id="B50-cancers-11-01802"><label>50.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xu</surname><given-names>S.</given-names></name><name><surname>Wan</surname><given-names>L.</given-names></name><name><surname>Yin</surname><given-names>H.</given-names></name><name><surname>Xu</surname><given-names>H.</given-names></name><name><surname>Zheng</surname><given-names>W.</given-names></name><name><surname>Shen</surname><given-names>M.</given-names></name><name><surname>Zhang</surname><given-names>Z.</given-names></name><name><surname>Pang</surname><given-names>D.</given-names></name></person-group><article-title>Long Noncoding RNA Linc00152 Functions as a Tumor Propellant in Pan-Cancer</article-title><source>Cell. Physiol. Biochem.</source><year>2017</year><volume>44</volume><fpage>2476</fpage><lpage>2490</lpage><pub-id pub-id-type="doi">10.1159/000486170</pub-id><pub-id pub-id-type="pmid">29268251</pub-id></element-citation></ref><ref id="B51-cancers-11-01802"><label>51.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>Y.</given-names></name><name><surname>Ren</surname><given-names>M.</given-names></name><name><surname>Song</surname><given-names>C.</given-names></name><name><surname>Li</surname><given-names>D.</given-names></name><name><surname>Soomro</surname><given-names>S.H.</given-names></name><name><surname>Xiong</surname><given-names>Y.</given-names></name><name><surname>Zhang</surname><given-names>H.</given-names></name><name><surname>Fu</surname><given-names>H.</given-names></name></person-group><article-title>LINC00461, a long non-coding RNA, is important for the proliferation and migration of glioma cells</article-title><source>Oncotarget</source><year>2017</year><volume>8</volume><fpage>84123</fpage><lpage>84139</lpage><pub-id pub-id-type="doi">10.18632/oncotarget.20340</pub-id><pub-id pub-id-type="pmid">29137410</pub-id></element-citation></ref><ref id="B52-cancers-11-01802"><label>52.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shim</surname><given-names>H.S.</given-names></name><name><surname>Yoon</surname><given-names>B.S.</given-names></name><name><surname>Cho</surname><given-names>N.H.</given-names></name></person-group><article-title>Prognostic significance of paired epithelial cell adhesion molecule and E-cadherin in ovarian serous carcinoma</article-title><source>Hum. Pathol.</source><year>2009</year><volume>40</volume><fpage>693</fpage><lpage>698</lpage><pub-id pub-id-type="doi">10.1016/j.humpath.2008.10.013</pub-id><pub-id pub-id-type="pmid">19157508</pub-id></element-citation></ref><ref id="B53-cancers-11-01802"><label>53.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dong</surname><given-names>L.</given-names></name><name><surname>Qian</surname><given-names>J.</given-names></name><name><surname>Chen</surname><given-names>F.</given-names></name><name><surname>Fan</surname><given-names>Y.</given-names></name><name><surname>Long</surname><given-names>J.</given-names></name></person-group><article-title>LINC00461 promotes cell migration and invasion in breast cancer through miR-30a-5p/integrin beta3 axis</article-title><source>J. Cell. Biochem.</source><year>2019</year><volume>120</volume><fpage>4851</fpage><lpage>4862</lpage><pub-id pub-id-type="doi">10.1002/jcb.27435</pub-id><pub-id pub-id-type="pmid">30623482</pub-id></element-citation></ref><ref id="B54-cancers-11-01802"><label>54.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Murakami</surname><given-names>A.</given-names></name><name><surname>Nakagawa</surname><given-names>T.</given-names></name><name><surname>Fukushima</surname><given-names>C.</given-names></name><name><surname>Torii</surname><given-names>M.</given-names></name><name><surname>Sueoka</surname><given-names>K.</given-names></name><name><surname>Nawata</surname><given-names>S.</given-names></name><name><surname>Takeda</surname><given-names>O.</given-names></name><name><surname>Ishikawa</surname><given-names>H.</given-names></name><name><surname>Sugino</surname><given-names>N.</given-names></name></person-group><article-title>Relationship between decreased expression of squamous cell carcinoma antigen 2 and E-cadherin in primary cervical cancer lesions and lymph node metastasis</article-title><source>Oncol. Rep.</source><year>2008</year><volume>19</volume><fpage>99</fpage><lpage>104</lpage><pub-id pub-id-type="doi">10.3892/or.19.1.99</pub-id><pub-id pub-id-type="pmid">18097581</pub-id></element-citation></ref><ref id="B55-cancers-11-01802"><label>55.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shi</surname><given-names>Y.</given-names></name><name><surname>Ye</surname><given-names>P.</given-names></name><name><surname>Long</surname><given-names>X.</given-names></name></person-group><article-title>Differential Expression Profiles of the Transcriptome in Breast Cancer Cell Lines Revealed by Next Generation Sequencing</article-title><source>Cell. Physiol. Biochem.</source><year>2017</year><volume>44</volume><fpage>804</fpage><lpage>816</lpage><pub-id pub-id-type="doi">10.1159/000485344</pub-id><pub-id pub-id-type="pmid">29176322</pub-id></element-citation></ref><ref id="B56-cancers-11-01802"><label>56.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jia</surname><given-names>Y.</given-names></name><name><surname>Shi</surname><given-names>L.</given-names></name><name><surname>Yun</surname><given-names>F.</given-names></name><name><surname>Liu</surname><given-names>X.</given-names></name><name><surname>Chen</surname><given-names>Y.</given-names></name><name><surname>Wang</surname><given-names>M.</given-names></name><name><surname>Chen</surname><given-names>C.</given-names></name><name><surname>Ren</surname><given-names>Y.</given-names></name><name><surname>Bao</surname><given-names>Y.</given-names></name><name><surname>Wang</surname><given-names>L.</given-names></name></person-group><article-title>Transcriptome sequencing profiles reveal lncRNAs may involve in breast cancer (ER/PR positive type) by interaction with RAS associated genes</article-title><source>Pathol. Res. Pract.</source><year>2019</year><volume>215</volume><fpage>152405</fpage><pub-id pub-id-type="doi">10.1016/j.prp.2019.03.033</pub-id><pub-id pub-id-type="pmid">30981459</pub-id></element-citation></ref><ref id="B57-cancers-11-01802"><label>57.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>M.</given-names></name><name><surname>Wu</surname><given-names>W.B.</given-names></name><name><surname>Wang</surname><given-names>Z.W.</given-names></name><name><surname>Wang</surname><given-names>X.H.</given-names></name></person-group><article-title>lncRNA NEAT1 is closely related with progression of breast cancer via promoting proliferation and EMT</article-title><source>Eur. Rev. Med. Pharmacol. Sci.</source><year>2017</year><volume>21</volume><fpage>1020</fpage><lpage>1026</lpage><pub-id pub-id-type="pmid">28338194</pub-id></element-citation></ref><ref id="B58-cancers-11-01802"><label>58.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jiang</surname><given-names>X.</given-names></name><name><surname>Zhou</surname><given-names>Y.</given-names></name><name><surname>Sun</surname><given-names>A.J.</given-names></name><name><surname>Xue</surname><given-names>J.L.</given-names></name></person-group><article-title>NEAT1 contributes to breast cancer progression through modulating miR-448 and ZEB1</article-title><source>J. Cell. Physiol.</source><year>2018</year><volume>233</volume><fpage>8558</fpage><lpage>8566</lpage><pub-id pub-id-type="doi">10.1002/jcp.26470</pub-id><pub-id pub-id-type="pmid">29323713</pub-id></element-citation></ref><ref id="B59-cancers-11-01802"><label>59.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shin</surname><given-names>V.Y.</given-names></name><name><surname>Chen</surname><given-names>J.</given-names></name><name><surname>Cheuk</surname><given-names>I.W.</given-names></name><name><surname>Siu</surname><given-names>M.T.</given-names></name><name><surname>Ho</surname><given-names>C.W.</given-names></name><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Jin</surname><given-names>H.</given-names></name><name><surname>Kwong</surname><given-names>A.</given-names></name></person-group><article-title>Long non-coding RNA NEAT1 confers oncogenic role in triple-negative breast cancer through modulating chemoresistance and cancer stemness</article-title><source>Cell Death Dis.</source><year>2019</year><volume>10</volume><fpage>270</fpage><pub-id pub-id-type="doi">10.1038/s41419-019-1513-5</pub-id><pub-id pub-id-type="pmid">30894512</pub-id></element-citation></ref><ref id="B60-cancers-11-01802"><label>60.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xiong</surname><given-names>Y.</given-names></name><name><surname>Gu</surname><given-names>Y.</given-names></name><name><surname>Wang</surname><given-names>F.</given-names></name><name><surname>Li</surname><given-names>L.</given-names></name><name><surname>Zhu</surname><given-names>M.</given-names></name><name><surname>Wang</surname><given-names>N.</given-names></name><name><surname>Mi</surname><given-names>H.</given-names></name><name><surname>Qiu</surname><given-names>X.</given-names></name></person-group><article-title>LINC01857 as an oncogene regulates CREB1 activation by interacting with CREBBP in breast cancer</article-title><source>J. Cell. Physiol.</source><year>2019</year><pub-id pub-id-type="doi">10.1002/jcp.28090</pub-id></element-citation></ref><ref id="B61-cancers-11-01802"><label>61.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jia</surname><given-names>D.</given-names></name><name><surname>Augert</surname><given-names>A.</given-names></name><name><surname>Kim</surname><given-names>D.</given-names></name><name><surname>Eastwood</surname><given-names>E.</given-names></name><name><surname>Wu</surname><given-names>N.</given-names></name><name><surname>Ibrahim</surname><given-names>A.</given-names></name><name><surname>Kim</surname><given-names>K.</given-names></name><name><surname>Dunn</surname><given-names>C.</given-names></name><name><surname>Pillai</surname><given-names>S.</given-names></name><name><surname>Gazdar</surname><given-names>A.</given-names></name><etal></etal></person-group><article-title>Loss Drives Small Cell Lung Cancer and Increases Sensitivity to HDAC Inhibition</article-title><source>Cancer Discov.</source><year>2018</year><volume>8</volume><fpage>1422</fpage><lpage>1437</lpage><pub-id pub-id-type="doi">10.1158/2159-8290.CD-18-0385</pub-id><pub-id pub-id-type="pmid">30181244</pub-id></element-citation></ref><ref id="B62-cancers-11-01802"><label>62.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Garcia-Carpizo</surname><given-names>V.</given-names></name><name><surname>Ruiz-Llorente</surname><given-names>S.</given-names></name><name><surname>Sarmentero</surname><given-names>J.</given-names></name><name><surname>González-Corpas</surname><given-names>A.</given-names></name><name><surname>Barrero</surname><given-names>M.</given-names></name></person-group><article-title>CREBBP/EP300 Bromodomain Inhibition Affects the Proliferation of AR-Positive Breast Cancer Cell Lines</article-title><source>Mol. Cancer Res. MCR</source><year>2019</year><volume>17</volume><fpage>720</fpage><lpage>730</lpage><pub-id pub-id-type="doi">10.1158/1541-7786.MCR-18-0719</pub-id><pub-id pub-id-type="pmid">30606771</pub-id></element-citation></ref><ref id="B63-cancers-11-01802"><label>63.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhou</surname><given-names>W.</given-names></name><name><surname>Ye</surname><given-names>X.L.</given-names></name><name><surname>Xu</surname><given-names>J.</given-names></name><name><surname>Cao</surname><given-names>M.G.</given-names></name><name><surname>Fang</surname><given-names>Z.Y.</given-names></name><name><surname>Li</surname><given-names>L.Y.</given-names></name><name><surname>Guan</surname><given-names>G.H.</given-names></name><name><surname>Liu</surname><given-names>Q.</given-names></name><name><surname>Qian</surname><given-names>Y.H.</given-names></name><name><surname>Xie</surname><given-names>D.</given-names></name></person-group><article-title>The lncRNA H19 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b</article-title><source>Sci. Signal.</source><year>2017</year><volume>10</volume><pub-id pub-id-type="doi">10.1126/scisignal.aak9557</pub-id><pub-id pub-id-type="pmid">28611183</pub-id></element-citation></ref><ref id="B64-cancers-11-01802"><label>64.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ocaña</surname><given-names>O.</given-names></name><name><surname>Córcoles</surname><given-names>R.</given-names></name><name><surname>Fabra</surname><given-names>A.</given-names></name><name><surname>Moreno-Bueno</surname><given-names>G.</given-names></name><name><surname>Acloque</surname><given-names>H.</given-names></name><name><surname>Vega</surname><given-names>S.</given-names></name><name><surname>Barrallo-Gimeno</surname><given-names>A.</given-names></name><name><surname>Cano</surname><given-names>A.</given-names></name><name><surname>Nieto</surname><given-names>M.</given-names></name></person-group><article-title>Metastatic colonization requires the repression of the epithelial-mesenchymal transition inducer Prrx1</article-title><source>Cancer Cell</source><year>2012</year><volume>22</volume><fpage>709</fpage><lpage>724</lpage><pub-id pub-id-type="doi">10.1016/j.ccr.2012.10.012</pub-id><pub-id pub-id-type="pmid">23201163</pub-id></element-citation></ref><ref id="B65-cancers-11-01802"><label>65.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Beerling</surname><given-names>E.</given-names></name><name><surname>Seinstra</surname><given-names>D.</given-names></name><name><surname>de Wit</surname><given-names>E.</given-names></name><name><surname>Kester</surname><given-names>L.</given-names></name><name><surname>van der Velden</surname><given-names>D.</given-names></name><name><surname>Maynard</surname><given-names>C.</given-names></name><name><surname>Schäfer</surname><given-names>R.</given-names></name><name><surname>van Diest</surname><given-names>P.</given-names></name><name><surname>Voest</surname><given-names>E.</given-names></name><name><surname>van Oudenaarden</surname><given-names>A.</given-names></name><etal></etal></person-group><article-title>Plasticity between Epithelial and Mesenchymal States Unlinks EMT from Metastasis-Enhancing Stem Cell Capacity</article-title><source>Cell Rep.</source><year>2016</year><volume>14</volume><fpage>2281</fpage><lpage>2288</lpage><pub-id pub-id-type="doi">10.1016/j.celrep.2016.02.034</pub-id><pub-id pub-id-type="pmid">26947068</pub-id></element-citation></ref><ref id="B66-cancers-11-01802"><label>66.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Matouk</surname><given-names>I.J.</given-names></name><name><surname>Raveh</surname><given-names>E.</given-names></name><name><surname>Abu-lail</surname><given-names>R.</given-names></name><name><surname>Mezan</surname><given-names>S.</given-names></name><name><surname>Gilon</surname><given-names>M.</given-names></name><name><surname>Gershtain</surname><given-names>E.</given-names></name><name><surname>Birman</surname><given-names>T.</given-names></name><name><surname>Gallula</surname><given-names>J.</given-names></name><name><surname>Schneider</surname><given-names>T.</given-names></name><name><surname>Barkali</surname><given-names>M.</given-names></name><etal></etal></person-group><article-title>Oncofetal H19 RNA promotes tumor metastasis</article-title><source>Biochim. Biophys. Acta</source><year>2014</year><volume>1843</volume><fpage>1414</fpage><lpage>1426</lpage><pub-id pub-id-type="doi">10.1016/j.bbamcr.2014.03.023</pub-id><pub-id pub-id-type="pmid">24703882</pub-id></element-citation></ref><ref id="B67-cancers-11-01802"><label>67.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lu</surname><given-names>R.</given-names></name><name><surname>Zhang</surname><given-names>J.</given-names></name><name><surname>Zhang</surname><given-names>W.</given-names></name><name><surname>Huang</surname><given-names>Y.</given-names></name><name><surname>Wang</surname><given-names>N.</given-names></name><name><surname>Zhang</surname><given-names>Q.</given-names></name><name><surname>Qu</surname><given-names>S.</given-names></name></person-group><article-title>Circulating HOTAIR expression predicts the clinical response to neoadjuvant chemotherapy in patients with breast cancer</article-title><source>Cancer Biomark.</source><year>2018</year><volume>22</volume><fpage>249</fpage><lpage>256</lpage><pub-id pub-id-type="doi">10.3233/CBM-170874</pub-id><pub-id pub-id-type="pmid">29630518</pub-id></element-citation></ref><ref id="B68-cancers-11-01802"><label>68.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Barkan</surname><given-names>D.</given-names></name><name><surname>Kleinman</surname><given-names>H.</given-names></name><name><surname>Simmons</surname><given-names>J.</given-names></name><name><surname>Asmussen</surname><given-names>H.</given-names></name><name><surname>Kamaraju</surname><given-names>A.</given-names></name><name><surname>Hoenorhoff</surname><given-names>M.</given-names></name><name><surname>Liu</surname><given-names>Z.</given-names></name><name><surname>Costes</surname><given-names>S.</given-names></name><name><surname>Cho</surname><given-names>E.</given-names></name><name><surname>Lockett</surname><given-names>S.</given-names></name><etal></etal></person-group><article-title>Inhibition of metastatic outgrowth from single dormant tumor cells by targeting the cytoskeleton</article-title><source>Cancer Res.</source><year>2008</year><volume>68</volume><fpage>6241</fpage><lpage>6250</lpage><pub-id pub-id-type="doi">10.1158/0008-5472.CAN-07-6849</pub-id><pub-id pub-id-type="pmid">18676848</pub-id></element-citation></ref><ref id="B69-cancers-11-01802"><label>69.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ren</surname><given-names>Y.</given-names></name><name><surname>Jia</surname><given-names>H.H.</given-names></name><name><surname>Xu</surname><given-names>Y.Q.</given-names></name><name><surname>Zhou</surname><given-names>X.</given-names></name><name><surname>Zhao</surname><given-names>X.H.</given-names></name><name><surname>Wang</surname><given-names>Y.F.</given-names></name><name><surname>Song</surname><given-names>X.</given-names></name><name><surname>Zhu</surname><given-names>Z.Y.</given-names></name><name><surname>Sun</surname><given-names>T.</given-names></name><name><surname>Dou</surname><given-names>Y.</given-names></name><etal></etal></person-group><article-title>Paracrine and epigenetic control of CAF-induced metastasis: The role of HOTAIR stimulated by TGF-ss1 secretion</article-title><source>Mol. Cancer</source><year>2018</year><volume>17</volume><fpage>5</fpage><pub-id pub-id-type="doi">10.1186/s12943-018-0758-4</pub-id><pub-id pub-id-type="pmid">29325547</pub-id></element-citation></ref><ref id="B70-cancers-11-01802"><label>70.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Teoh-Fitzgerald</surname><given-names>M.L.</given-names></name><name><surname>Fitzgerald</surname><given-names>M.P.</given-names></name><name><surname>Zhong</surname><given-names>W.</given-names></name><name><surname>Askeland</surname><given-names>R.W.</given-names></name><name><surname>Domann</surname><given-names>F.E.</given-names></name></person-group><article-title>Epigenetic reprogramming governs EcSOD expression during human mammary epithelial cell differentiation, tumorigenesis and metastasis</article-title><source>Oncogene</source><year>2014</year><volume>33</volume><fpage>358</fpage><lpage>368</lpage><pub-id pub-id-type="doi">10.1038/onc.2012.582</pub-id><pub-id pub-id-type="pmid">23318435</pub-id></element-citation></ref><ref id="B71-cancers-11-01802"><label>71.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lelièvre</surname><given-names>S.A.</given-names></name></person-group><article-title>Tissue polarity-dependent control of mammary epithelial homeostasis and cancer development: An epigenetic perspective</article-title><source>J. Mammary Gland Biol. Neoplasia</source><year>2010</year><volume>15</volume><fpage>49</fpage><lpage>63</lpage><pub-id pub-id-type="doi">10.1007/s10911-010-9168-y</pub-id><pub-id pub-id-type="pmid">20101444</pub-id></element-citation></ref><ref id="B72-cancers-11-01802"><label>72.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>M.</given-names></name><name><surname>Li</surname><given-names>X.</given-names></name><name><surname>Zhuang</surname><given-names>Y.</given-names></name><name><surname>Flemington</surname><given-names>E.K.</given-names></name><name><surname>Lin</surname><given-names>Z.</given-names></name><name><surname>Shan</surname><given-names>B.</given-names></name></person-group><article-title>Induction of a novel isoform of the lncRNA HOTAIR in Claudin-low breast cancer cells attached to extracellular matrix</article-title><source>Mol. Oncol.</source><year>2017</year><volume>11</volume><fpage>1698</fpage><lpage>1710</lpage><pub-id pub-id-type="doi">10.1002/1878-0261.12133</pub-id><pub-id pub-id-type="pmid">28846832</pub-id></element-citation></ref><ref id="B73-cancers-11-01802"><label>73.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gupta</surname><given-names>R.</given-names></name><name><surname>Shah</surname><given-names>N.</given-names></name><name><surname>Wang</surname><given-names>K.</given-names></name><name><surname>Kim</surname><given-names>J.</given-names></name><name><surname>Horlings</surname><given-names>H.</given-names></name><name><surname>Wong</surname><given-names>D.</given-names></name><name><surname>Tsai</surname><given-names>M.</given-names></name><name><surname>Hung</surname><given-names>T.</given-names></name><name><surname>Argani</surname><given-names>P.</given-names></name><name><surname>Rinn</surname><given-names>J.</given-names></name><etal></etal></person-group><article-title>Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis</article-title><source>Nature</source><year>2010</year><volume>464</volume><fpage>1071</fpage><lpage>1076</lpage><pub-id pub-id-type="doi">10.1038/nature08975</pub-id><pub-id pub-id-type="pmid">20393566</pub-id></element-citation></ref><ref id="B74-cancers-11-01802"><label>74.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wang</surname><given-names>Y.</given-names></name><name><surname>Zhang</surname><given-names>G.</given-names></name><name><surname>Han</surname><given-names>J.</given-names></name></person-group><article-title>HIF1A-AS2 predicts poor prognosis and regulates cell migration and invasion in triple-negative breast cancer</article-title><source>J. Cell. Biochem.</source><year>2019</year><pub-id pub-id-type="doi">10.1002/jcb.28337</pub-id><pub-id pub-id-type="pmid">30635931</pub-id></element-citation></ref><ref id="B75-cancers-11-01802"><label>75.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>M.</given-names></name><name><surname>Xing</surname><given-names>L.</given-names></name><name><surname>Liu</surname><given-names>Y.</given-names></name></person-group><article-title>A three-long noncoding RNA signature as a diagnostic biomarker for differentiating between triple-negative and non-triple-negative breast cancers</article-title><source>Medicine</source><year>2017</year><volume>96</volume><fpage>e6222</fpage><pub-id pub-id-type="doi">10.1097/MD.0000000000006222</pub-id><pub-id pub-id-type="pmid">28248879</pub-id></element-citation></ref><ref id="B76-cancers-11-01802"><label>76.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jia</surname><given-names>X.</given-names></name><name><surname>Shi</surname><given-names>L.</given-names></name><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Luo</surname><given-names>L.</given-names></name><name><surname>Ling</surname><given-names>L.</given-names></name><name><surname>Yin</surname><given-names>J.</given-names></name><name><surname>Song</surname><given-names>Y.</given-names></name><name><surname>Zhang</surname><given-names>Z.</given-names></name><name><surname>Qiu</surname><given-names>N.</given-names></name><name><surname>Liu</surname><given-names>H.</given-names></name><etal></etal></person-group><article-title>KLF5 regulated lncRNA RP1 promotes the growth and metastasis of breast cancer via repressing p27kip1 translation</article-title><source>Cell Death Dis.</source><year>2019</year><volume>10</volume><fpage>373</fpage><pub-id pub-id-type="doi">10.1038/s41419-019-1566-5</pub-id><pub-id pub-id-type="pmid">31073122</pub-id></element-citation></ref><ref id="B77-cancers-11-01802"><label>77.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>B.</given-names></name><name><surname>Arun</surname><given-names>G.</given-names></name><name><surname>Mao</surname><given-names>Y.S.</given-names></name><name><surname>Lazar</surname><given-names>Z.</given-names></name><name><surname>Hung</surname><given-names>G.</given-names></name><name><surname>Bhattacharjee</surname><given-names>G.</given-names></name><name><surname>Xiao</surname><given-names>X.</given-names></name><name><surname>Booth</surname><given-names>C.J.</given-names></name><name><surname>Wu</surname><given-names>J.</given-names></name><name><surname>Zhang</surname><given-names>C.</given-names></name><etal></etal></person-group><article-title>The lncRNA Malat1 is dispensable for mouse development but its transcription plays a cis-regulatory role in the adult</article-title><source>Cell Rep.</source><year>2012</year><volume>2</volume><fpage>111</fpage><lpage>123</lpage><pub-id pub-id-type="doi">10.1016/j.celrep.2012.06.003</pub-id><pub-id pub-id-type="pmid">22840402</pub-id></element-citation></ref><ref id="B78-cancers-11-01802"><label>78.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Miao</surname><given-names>Y.</given-names></name><name><surname>Fan</surname><given-names>R.</given-names></name><name><surname>Chen</surname><given-names>L.</given-names></name><name><surname>Qian</surname><given-names>H.</given-names></name></person-group><article-title>Clinical Significance of Long Non-coding RNA MALAT1 Expression in Tissue and Serum of Breast Cancer</article-title><source>Ann. Clin. Lab. Sci.</source><year>2016</year><volume>46</volume><fpage>418</fpage><lpage>424</lpage><pub-id pub-id-type="pmid">27466303</pub-id></element-citation></ref><ref id="B79-cancers-11-01802"><label>79.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jadaliha</surname><given-names>M.</given-names></name><name><surname>Zong</surname><given-names>X.</given-names></name><name><surname>Malakar</surname><given-names>P.</given-names></name><name><surname>Ray</surname><given-names>T.</given-names></name><name><surname>Singh</surname><given-names>D.K.</given-names></name><name><surname>Freier</surname><given-names>S.M.</given-names></name><name><surname>Jensen</surname><given-names>T.</given-names></name><name><surname>Prasanth</surname><given-names>S.G.</given-names></name><name><surname>Karni</surname><given-names>R.</given-names></name><name><surname>Ray</surname><given-names>P.S.</given-names></name><etal></etal></person-group><article-title>Functional and prognostic significance of long non-coding RNA MALAT1 as a metastasis driver in ER negative lymph node negative breast cancer</article-title><source>Oncotarget</source><year>2016</year><volume>7</volume><fpage>40418</fpage><lpage>40436</lpage><pub-id pub-id-type="doi">10.18632/oncotarget.9622</pub-id><pub-id pub-id-type="pmid">27250026</pub-id></element-citation></ref><ref id="B80-cancers-11-01802"><label>80.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jin</surname><given-names>C.</given-names></name><name><surname>Yan</surname><given-names>B.</given-names></name><name><surname>Lu</surname><given-names>Q.</given-names></name><name><surname>Lin</surname><given-names>Y.</given-names></name><name><surname>Ma</surname><given-names>L.</given-names></name></person-group><article-title>Reciprocal regulation of Hsa-miR-1 and long noncoding RNA MALAT1 promotes triple-negative breast cancer development</article-title><source>Tumour Biol. J. Int. Soc. Oncodev. Biol. Med.</source><year>2016</year><volume>37</volume><fpage>7383</fpage><lpage>7394</lpage><pub-id pub-id-type="doi">10.1007/s13277-015-4605-6</pub-id></element-citation></ref><ref id="B81-cancers-11-01802"><label>81.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>X.</given-names></name><name><surname>Chen</surname><given-names>N.</given-names></name><name><surname>Zhou</surname><given-names>L.</given-names></name><name><surname>Wang</surname><given-names>C.</given-names></name><name><surname>Wen</surname><given-names>X.</given-names></name><name><surname>Jia</surname><given-names>L.</given-names></name><name><surname>Cui</surname><given-names>J.</given-names></name><name><surname>Hoffman</surname><given-names>A.</given-names></name><name><surname>Hu</surname><given-names>J.</given-names></name><name><surname>Li</surname><given-names>W.</given-names></name></person-group><article-title>Genome-wide target interactome profiling reveals a novel epigenetic pathway for oncogenic lncRNA in breast cancer</article-title><source>Am. J. Cancer Res.</source><year>2019</year><volume>9</volume><fpage>714</fpage><lpage>729</lpage><pub-id pub-id-type="pmid">31105998</pub-id></element-citation></ref><ref id="B82-cancers-11-01802"><label>82.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>Z.</given-names></name><name><surname>Xu</surname><given-names>L.</given-names></name><name><surname>Liu</surname><given-names>Y.</given-names></name><name><surname>Fu</surname><given-names>S.</given-names></name><name><surname>Tu</surname><given-names>J.</given-names></name><name><surname>Hu</surname><given-names>Y.</given-names></name><name><surname>Xiong</surname><given-names>Q.</given-names></name></person-group><article-title>LncRNA MALAT1 promotes relapse of breast cancer patients with postoperative fever</article-title><source>Am. J. Transl. Res.</source><year>2018</year><volume>10</volume><fpage>3186</fpage><lpage>3197</lpage><pub-id pub-id-type="pmid">30416660</pub-id></element-citation></ref><ref id="B83-cancers-11-01802"><label>83.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Stone</surname><given-names>J.</given-names></name><name><surname>Kim</surname><given-names>J.</given-names></name><name><surname>Vukadin</surname><given-names>L.</given-names></name><name><surname>Richard</surname><given-names>A.</given-names></name><name><surname>Giannini</surname><given-names>H.</given-names></name><name><surname>Lim</surname><given-names>S.</given-names></name><name><surname>Tan</surname><given-names>M.</given-names></name><name><surname>Ahn</surname><given-names>E.</given-names></name></person-group><article-title>Hypoxia induces cancer cell-specific chromatin interactions and increases MALAT1 expression in breast cancer cells</article-title><source>J. Biol. Chem.</source><year>2019</year><volume>294</volume><fpage>11213</fpage><lpage>11224</lpage><pub-id pub-id-type="doi">10.1074/jbc.RA118.006889</pub-id><pub-id pub-id-type="pmid">31167784</pub-id></element-citation></ref><ref id="B84-cancers-11-01802"><label>84.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Arun</surname><given-names>G.</given-names></name><name><surname>Diermeier</surname><given-names>S.</given-names></name><name><surname>Akerman</surname><given-names>M.</given-names></name><name><surname>Chang</surname><given-names>K.</given-names></name><name><surname>Wilkinson</surname><given-names>J.</given-names></name><name><surname>Hearn</surname><given-names>S.</given-names></name><name><surname>Kim</surname><given-names>Y.</given-names></name><name><surname>MacLeod</surname><given-names>A.</given-names></name><name><surname>Krainer</surname><given-names>A.</given-names></name><name><surname>Norton</surname><given-names>L.</given-names></name><etal></etal></person-group><article-title>Differentiation of mammary tumors and reduction in metastasis upon Malat1 lncRNA loss</article-title><source>Genes Dev.</source><year>2016</year><volume>30</volume><fpage>34</fpage><lpage>51</lpage><pub-id pub-id-type="doi">10.1101/gad.270959.115</pub-id><pub-id pub-id-type="pmid">26701265</pub-id></element-citation></ref><ref id="B85-cancers-11-01802"><label>85.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zuo</surname><given-names>Y.</given-names></name><name><surname>Li</surname><given-names>Y.</given-names></name><name><surname>Zhou</surname><given-names>Z.</given-names></name><name><surname>Ma</surname><given-names>M.</given-names></name><name><surname>Fu</surname><given-names>K.</given-names></name></person-group><article-title>Long non-coding RNA MALAT1 promotes proliferation and invasion via targeting miR-129-5p in triple-negative breast cancer</article-title><source>Biomed. Pharmacother.</source><year>2017</year><volume>95</volume><fpage>922</fpage><lpage>928</lpage><pub-id pub-id-type="doi">10.1016/j.biopha.2017.09.005</pub-id><pub-id pub-id-type="pmid">28915533</pub-id></element-citation></ref><ref id="B86-cancers-11-01802"><label>86.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Schneider</surname><given-names>C.</given-names></name><name><surname>King</surname><given-names>R.M.</given-names></name><name><surname>Philipson</surname><given-names>L.</given-names></name></person-group><article-title>Genes specifically expressed at growth arrest of mammalian cells</article-title><source>Cell</source><year>1988</year><volume>54</volume><fpage>787</fpage><lpage>793</lpage><pub-id pub-id-type="doi">10.1016/S0092-8674(88)91065-3</pub-id><pub-id pub-id-type="pmid">3409319</pub-id></element-citation></ref><ref id="B87-cancers-11-01802"><label>87.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Arshi</surname><given-names>A.</given-names></name><name><surname>Sharifi</surname><given-names>F.S.</given-names></name><name><surname>Khorramian Ghahfarokhi</surname><given-names>M.</given-names></name><name><surname>Faghih</surname><given-names>Z.</given-names></name><name><surname>Doosti</surname><given-names>A.</given-names></name><name><surname>Ostovari</surname><given-names>S.</given-names></name><name><surname>Mahmoudi Maymand</surname><given-names>E.</given-names></name><name><surname>Ghahramani Seno</surname><given-names>M.M.</given-names></name></person-group><article-title>Expression Analysis of MALAT1, GAS5, SRA, and NEAT1 lncRNAs in Breast Cancer Tissues from Young Women and Women over 45 Years of Age</article-title><source>Mol. Nucleic Acids</source><year>2018</year><volume>12</volume><fpage>751</fpage><lpage>757</lpage><pub-id pub-id-type="doi">10.1016/j.omtn.2018.07.014</pub-id><pub-id pub-id-type="pmid">30126830</pub-id></element-citation></ref><ref id="B88-cancers-11-01802"><label>88.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>Z.</given-names></name><name><surname>Zhu</surname><given-names>Z.</given-names></name><name><surname>Watabe</surname><given-names>K.</given-names></name><name><surname>Zhang</surname><given-names>X.</given-names></name><name><surname>Bai</surname><given-names>C.</given-names></name><name><surname>Xu</surname><given-names>M.</given-names></name><name><surname>Wu</surname><given-names>F.</given-names></name><name><surname>Mo</surname><given-names>Y.Y.</given-names></name></person-group><article-title>Negative regulation of lncRNA GAS5 by miR-21</article-title><source>Cell Death Differ.</source><year>2013</year><volume>20</volume><fpage>1558</fpage><lpage>1568</lpage><pub-id pub-id-type="doi">10.1038/cdd.2013.110</pub-id><pub-id pub-id-type="pmid">23933812</pub-id></element-citation></ref><ref id="B89-cancers-11-01802"><label>89.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>S.</given-names></name><name><surname>Zhou</surname><given-names>J.</given-names></name><name><surname>Wang</surname><given-names>Z.</given-names></name><name><surname>Wang</surname><given-names>P.</given-names></name><name><surname>Gao</surname><given-names>X.</given-names></name><name><surname>Wang</surname><given-names>Y.</given-names></name></person-group><article-title>Long noncoding RNA GAS5 suppresses triple negative breast cancer progression through inhibition of proliferation and invasion by competitively binding miR-196a-5p</article-title><source>Biomed. Pharm.</source><year>2018</year><volume>104</volume><fpage>451</fpage><lpage>457</lpage><pub-id pub-id-type="doi">10.1016/j.biopha.2018.05.056</pub-id></element-citation></ref><ref id="B90-cancers-11-01802"><label>90.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>L.</given-names></name><name><surname>Yue</surname><given-names>H.</given-names></name><name><surname>Liu</surname><given-names>Q.</given-names></name><name><surname>Yuan</surname><given-names>J.</given-names></name><name><surname>Li</surname><given-names>J.</given-names></name><name><surname>Wei</surname><given-names>G.</given-names></name><name><surname>Chen</surname><given-names>X.</given-names></name><name><surname>Lu</surname><given-names>Y.</given-names></name><name><surname>Guo</surname><given-names>M.</given-names></name><name><surname>Luo</surname><given-names>J.</given-names></name><etal></etal></person-group><article-title>LncRNA MT1JP functions as a tumor suppressor by interacting with TIAR to modulate the p53 pathway</article-title><source>Oncotarget</source><year>2016</year><volume>7</volume><fpage>15787</fpage><lpage>15800</lpage><pub-id pub-id-type="doi">10.18632/oncotarget.7487</pub-id><pub-id pub-id-type="pmid">26909858</pub-id></element-citation></ref><ref id="B91-cancers-11-01802"><label>91.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xu</surname><given-names>Y.</given-names></name><name><surname>Zhang</surname><given-names>G.</given-names></name><name><surname>Zou</surname><given-names>C.</given-names></name><name><surname>Zhang</surname><given-names>H.</given-names></name><name><surname>Gong</surname><given-names>Z.</given-names></name><name><surname>Wang</surname><given-names>W.</given-names></name><name><surname>Ma</surname><given-names>G.</given-names></name><name><surname>Jiang</surname><given-names>P.</given-names></name><name><surname>Zhang</surname><given-names>W.</given-names></name></person-group><article-title>LncRNA MT1JP Suppresses Gastric Cancer Cell Proliferation and Migration Through MT1JP/MiR-214-3p/RUNX3 Axis</article-title><source>Cell. Physiol. Biochem. Int. J. Exp. Cell. Physiol. Biochem. Pharmacol.</source><year>2018</year><volume>46</volume><fpage>2445</fpage><lpage>2459</lpage><pub-id pub-id-type="doi">10.1159/000489651</pub-id></element-citation></ref><ref id="B92-cancers-11-01802"><label>92.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>G.</given-names></name><name><surname>Li</surname><given-names>S.</given-names></name><name><surname>Lu</surname><given-names>J.</given-names></name><name><surname>Ge</surname><given-names>Y.</given-names></name><name><surname>Wang</surname><given-names>Q.</given-names></name><name><surname>Ma</surname><given-names>G.</given-names></name><name><surname>Zhao</surname><given-names>Q.</given-names></name><name><surname>Wu</surname><given-names>D.</given-names></name><name><surname>Gong</surname><given-names>W.</given-names></name><name><surname>Du</surname><given-names>M.</given-names></name><etal></etal></person-group><article-title>LncRNA MT1JP functions as a ceRNA in regulating FBXW7 through competitively binding to miR-92a-3p in gastric cancer</article-title><source>Mol. Cancer</source><year>2018</year><volume>17</volume><fpage>87</fpage><pub-id pub-id-type="doi">10.1186/s12943-018-0829-6</pub-id><pub-id pub-id-type="pmid">29720189</pub-id></element-citation></ref><ref id="B93-cancers-11-01802"><label>93.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhu</surname><given-names>D.</given-names></name><name><surname>Zhang</surname><given-names>X.</given-names></name><name><surname>Lin</surname><given-names>Y.</given-names></name><name><surname>Liang</surname><given-names>S.</given-names></name><name><surname>Song</surname><given-names>Z.</given-names></name><name><surname>Dong</surname><given-names>C.</given-names></name></person-group><article-title>MT1JP inhibits tumorigenesis and enhances cisplatin sensitivity of breast cancer cells through competitively binding to miR-24-3p</article-title><source>Am. J. Transl. Res.</source><year>2019</year><volume>11</volume><fpage>245</fpage><lpage>256</lpage><pub-id pub-id-type="pmid">30787983</pub-id></element-citation></ref><ref id="B94-cancers-11-01802"><label>94.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liang</surname><given-names>Z.</given-names></name><name><surname>Zhu</surname><given-names>B.</given-names></name><name><surname>Meng</surname><given-names>D.</given-names></name><name><surname>Shen</surname><given-names>X.</given-names></name><name><surname>Li</surname><given-names>X.</given-names></name><name><surname>Wang</surname><given-names>Z.</given-names></name><name><surname>Li</surname><given-names>L.</given-names></name></person-group><article-title>Downregulation of lncRNA-NEF indicates poor prognosis in intrahepatic cholangiocarcinoma</article-title><source>Biosci. Rep.</source><year>2019</year><pub-id pub-id-type="doi">10.1042/BSR20181573</pub-id><pub-id pub-id-type="pmid">31015363</pub-id></element-citation></ref><ref id="B95-cancers-11-01802"><label>95.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chang</surname><given-names>L.</given-names></name><name><surname>Xu</surname><given-names>W.</given-names></name><name><surname>Zhang</surname><given-names>Y.</given-names></name><name><surname>Gong</surname><given-names>F.</given-names></name></person-group><article-title>Long non-coding RNA-NEF targets glucose transportation to inhibit the proliferation of non-small-cell lung cancer cells</article-title><source>Oncol. Lett.</source><year>2019</year><volume>17</volume><fpage>2795</fpage><lpage>2801</lpage><pub-id pub-id-type="doi">10.3892/ol.2019.9919</pub-id><pub-id pub-id-type="pmid">30854054</pub-id></element-citation></ref><ref id="B96-cancers-11-01802"><label>96.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liang</surname><given-names>W.C.</given-names></name><name><surname>Ren</surname><given-names>J.L.</given-names></name><name><surname>Wong</surname><given-names>C.W.</given-names></name><name><surname>Chan</surname><given-names>S.O.</given-names></name><name><surname>Waye</surname><given-names>M.M.</given-names></name><name><surname>Fu</surname><given-names>W.M.</given-names></name><name><surname>Zhang</surname><given-names>J.F.</given-names></name></person-group><article-title>LncRNA-NEF antagonized epithelial to mesenchymal transition and cancer metastasis via cis-regulating FOXA2 and inactivating Wnt/beta-catenin signaling</article-title><source>Oncogene</source><year>2018</year><volume>37</volume><fpage>1445</fpage><lpage>1456</lpage><pub-id pub-id-type="doi">10.1038/s41388-017-0041-y</pub-id><pub-id pub-id-type="pmid">29311643</pub-id></element-citation></ref><ref id="B97-cancers-11-01802"><label>97.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Song</surname><given-names>X.</given-names></name><name><surname>Liu</surname><given-names>Z.</given-names></name><name><surname>Yu</surname><given-names>Z.</given-names></name></person-group><article-title>LncRNA NEF is downregulated in triple negative breast cancer and correlated with poor prognosis</article-title><source>Acta Biochim. Biophys. Sin.</source><year>2019</year><volume>51</volume><fpage>386</fpage><lpage>392</lpage><pub-id pub-id-type="doi">10.1093/abbs/gmz021</pub-id><pub-id pub-id-type="pmid">30839051</pub-id></element-citation></ref><ref id="B98-cancers-11-01802"><label>98.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ke</surname><given-names>S.</given-names></name><name><surname>Li</surname><given-names>R.C.</given-names></name><name><surname>Meng</surname><given-names>F.K.</given-names></name><name><surname>Fang</surname><given-names>M.H.</given-names></name></person-group><article-title>NKILA inhibits NF-kappaB signaling and suppresses tumor metastasis</article-title><source>Aging</source><year>2018</year><volume>10</volume><fpage>56</fpage><lpage>71</lpage><pub-id pub-id-type="doi">10.18632/aging.101359</pub-id><pub-id pub-id-type="pmid">29348395</pub-id></element-citation></ref><ref id="B99-cancers-11-01802"><label>99.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wu</surname><given-names>W.</given-names></name><name><surname>Chen</surname><given-names>F.</given-names></name><name><surname>Cui</surname><given-names>X.</given-names></name><name><surname>Yang</surname><given-names>L.</given-names></name><name><surname>Chen</surname><given-names>J.</given-names></name><name><surname>Zhao</surname><given-names>J.</given-names></name><name><surname>Huang</surname><given-names>D.</given-names></name><name><surname>Liu</surname><given-names>J.</given-names></name><name><surname>Yang</surname><given-names>L.</given-names></name><name><surname>Zeng</surname><given-names>J.</given-names></name><etal></etal></person-group><article-title>LncRNA NKILA suppresses TGF-beta-induced epithelial-mesenchymal transition by blocking NF-kappaB signaling in breast cancer</article-title><source>Int. J. Cancer</source><year>2018</year><volume>143</volume><fpage>2213</fpage><lpage>2224</lpage><pub-id pub-id-type="doi">10.1002/ijc.31605</pub-id><pub-id pub-id-type="pmid">29761481</pub-id></element-citation></ref><ref id="B100-cancers-11-01802"><label>100.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>B.</given-names></name><name><surname>Sun</surname><given-names>L.</given-names></name><name><surname>Liu</surname><given-names>Q.</given-names></name><name><surname>Gong</surname><given-names>C.</given-names></name><name><surname>Yao</surname><given-names>Y.</given-names></name><name><surname>Lv</surname><given-names>X.</given-names></name><name><surname>Lin</surname><given-names>L.</given-names></name><name><surname>Yao</surname><given-names>H.</given-names></name><name><surname>Su</surname><given-names>F.</given-names></name><name><surname>Li</surname><given-names>D.</given-names></name><etal></etal></person-group><article-title>A cytoplasmic NF-κB interacting long noncoding RNA blocks IκB phosphorylation and suppresses breast cancer metastasis</article-title><source>Cancer Cell</source><year>2015</year><volume>27</volume><fpage>370</fpage><lpage>381</lpage><pub-id pub-id-type="doi">10.1016/j.ccell.2015.02.004</pub-id><pub-id pub-id-type="pmid">25759022</pub-id></element-citation></ref><ref id="B101-cancers-11-01802"><label>101.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhou</surname><given-names>C.X.</given-names></name><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Yang</surname><given-names>N.</given-names></name><name><surname>Xue</surname><given-names>S.K.</given-names></name><name><surname>Li</surname><given-names>W.C.</given-names></name><name><surname>Xie</surname><given-names>P.P.</given-names></name></person-group><article-title>LncRNA LET function as a tumor suppressor in breast cancer development</article-title><source>Eur. Rev. Med. Pharmacol. Sci.</source><year>2018</year><volume>22</volume><fpage>6002</fpage><lpage>6007</lpage><pub-id pub-id-type="pmid">30280783</pub-id></element-citation></ref><ref id="B102-cancers-11-01802"><label>102.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhou</surname><given-names>B.</given-names></name><name><surname>Guo</surname><given-names>H.</given-names></name><name><surname>Tang</surname><given-names>J.</given-names></name></person-group><article-title>Long Non-Coding RNA TFAP2A-AS1 Inhibits Cell Proliferation and Invasion in Breast Cancer via miR-933/SMAD2</article-title><source>Med. Sci. Monit.</source><year>2019</year><volume>25</volume><fpage>1242</fpage><lpage>1253</lpage><pub-id pub-id-type="doi">10.12659/MSM.912421</pub-id><pub-id pub-id-type="pmid">30768589</pub-id></element-citation></ref><ref id="B103-cancers-11-01802"><label>103.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Beltran-Anaya</surname><given-names>F.O.</given-names></name><name><surname>Romero-Cordoba</surname><given-names>S.</given-names></name><name><surname>Rebollar-Vega</surname><given-names>R.</given-names></name><name><surname>Arrieta</surname><given-names>O.</given-names></name><name><surname>Bautista-Pina</surname><given-names>V.</given-names></name><name><surname>Dominguez-Reyes</surname><given-names>C.</given-names></name><name><surname>Villegas-Carlos</surname><given-names>F.</given-names></name><name><surname>Tenorio-Torres</surname><given-names>A.</given-names></name><name><surname>Alfaro-Riuz</surname><given-names>L.</given-names></name><name><surname>Jimenez-Morales</surname><given-names>S.</given-names></name><etal></etal></person-group><article-title>Expression of long non-coding RNA ENSG00000226738 (LncKLHDC7B) is enriched in the immunomodulatory triple-negative breast cancer subtype and its alteration promotes cell migration, invasion, and resistance to cell death</article-title><source>Mol. Oncol.</source><year>2019</year><pub-id pub-id-type="doi">10.1002/1878-0261.12446</pub-id><pub-id pub-id-type="pmid">30648789</pub-id></element-citation></ref><ref id="B104-cancers-11-01802"><label>104.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Curtis</surname><given-names>C.</given-names></name><name><surname>Shah</surname><given-names>S.</given-names></name><name><surname>Chin</surname><given-names>S.</given-names></name><name><surname>Turashvili</surname><given-names>G.</given-names></name><name><surname>Rueda</surname><given-names>O.</given-names></name><name><surname>Dunning</surname><given-names>M.</given-names></name><name><surname>Speed</surname><given-names>D.</given-names></name><name><surname>Lynch</surname><given-names>A.</given-names></name><name><surname>Samarajiwa</surname><given-names>S.</given-names></name><name><surname>Yuan</surname><given-names>Y.</given-names></name><etal></etal></person-group><article-title>The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups</article-title><source>Nature</source><year>2012</year><volume>486</volume><fpage>346</fpage><lpage>352</lpage><pub-id pub-id-type="doi">10.1038/nature10983</pub-id><pub-id pub-id-type="pmid">22522925</pub-id></element-citation></ref><ref id="B105-cancers-11-01802"><label>105.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lánczky</surname><given-names>A.</given-names></name><name><surname>Nagy</surname><given-names>Á.</given-names></name><name><surname>Bottai</surname><given-names>G.</given-names></name><name><surname>Munkácsy</surname><given-names>G.</given-names></name><name><surname>Szabó</surname><given-names>A.</given-names></name><name><surname>Santarpia</surname><given-names>L.</given-names></name><name><surname>Győrffy</surname><given-names>B.</given-names></name></person-group><article-title>miRpower: A web-tool to validate survival-associated miRNAs utilizing expression data from 2178 breast cancer patients</article-title><source>Breast Cancer Res. Treat.</source><year>2016</year><volume>160</volume><fpage>439</fpage><lpage>446</lpage><pub-id pub-id-type="doi">10.1007/s10549-016-4013-7</pub-id><pub-id pub-id-type="pmid">27744485</pub-id></element-citation></ref><ref id="B106-cancers-11-01802"><label>106.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Anaya</surname><given-names>J.</given-names></name></person-group><article-title>OncoLnc: Linking TCGA survival data to mRNAs, miRNAs, and lncRNAs</article-title><source>Peerj Comput. Sci.</source><year>2016</year><volume>2</volume><fpage>e67</fpage><pub-id pub-id-type="doi">10.7717/peerj-cs.67</pub-id></element-citation></ref><ref id="B107-cancers-11-01802"><label>107.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kim</surname><given-names>J.</given-names></name><name><surname>Piao</surname><given-names>H.</given-names></name><name><surname>Kim</surname><given-names>B.</given-names></name><name><surname>Yao</surname><given-names>F.</given-names></name><name><surname>Han</surname><given-names>Z.</given-names></name><name><surname>Wang</surname><given-names>Y.</given-names></name><name><surname>Xiao</surname><given-names>Z.</given-names></name><name><surname>Siverly</surname><given-names>A.</given-names></name><name><surname>Lawhon</surname><given-names>S.</given-names></name><name><surname>Ton</surname><given-names>B.</given-names></name><etal></etal></person-group><article-title>Long noncoding RNA MALAT1 suppresses breast cancer metastasis</article-title><source>Nat. Genet.</source><year>2018</year><volume>50</volume><fpage>1705</fpage><lpage>1715</lpage><pub-id pub-id-type="doi">10.1038/s41588-018-0252-3</pub-id><pub-id pub-id-type="pmid">30349115</pub-id></element-citation></ref><ref id="B108-cancers-11-01802"><label>108.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xu</surname><given-names>S.</given-names></name><name><surname>Sui</surname><given-names>S.</given-names></name><name><surname>Zhang</surname><given-names>J.</given-names></name><name><surname>Bai</surname><given-names>N.</given-names></name><name><surname>Shi</surname><given-names>Q.</given-names></name><name><surname>Zhang</surname><given-names>G.</given-names></name><name><surname>Gao</surname><given-names>S.</given-names></name><name><surname>You</surname><given-names>Z.</given-names></name><name><surname>Zhan</surname><given-names>C.</given-names></name><name><surname>Liu</surname><given-names>F.</given-names></name><etal></etal></person-group><article-title>Downregulation of long noncoding RNA MALAT1 induces epithelial-to-mesenchymal transition via the PI3K-AKT pathway in breast cancer</article-title><source>Int. J. Clin. Exp. Pathol.</source><year>2015</year><volume>8</volume><fpage>4881</fpage><lpage>4891</lpage><pub-id pub-id-type="pmid">26191181</pub-id></element-citation></ref><ref id="B109-cancers-11-01802"><label>109.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kwok</surname><given-names>Z.H.</given-names></name><name><surname>Roche</surname><given-names>V.</given-names></name><name><surname>Chew</surname><given-names>X.H.</given-names></name><name><surname>Fadieieva</surname><given-names>A.</given-names></name><name><surname>Tay</surname><given-names>Y.</given-names></name></person-group><article-title>A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers</article-title><source>Int. J. Cancer</source><year>2018</year><volume>143</volume><fpage>668</fpage><lpage>678</lpage><pub-id pub-id-type="doi">10.1002/ijc.31386</pub-id><pub-id pub-id-type="pmid">29574704</pub-id></element-citation></ref><ref id="B110-cancers-11-01802"><label>110.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chen</surname><given-names>Z.</given-names></name><name><surname>Liu</surname><given-names>S.</given-names></name><name><surname>Tian</surname><given-names>L.</given-names></name><name><surname>Wu</surname><given-names>M.</given-names></name><name><surname>Ai</surname><given-names>F.</given-names></name><name><surname>Tang</surname><given-names>W.</given-names></name><name><surname>Zhao</surname><given-names>L.</given-names></name><name><surname>Ding</surname><given-names>J.</given-names></name><name><surname>Zhang</surname><given-names>L.</given-names></name><name><surname>Tang</surname><given-names>A.</given-names></name></person-group><article-title>miR-124 and miR-506 inhibit colorectal cancer progression by targeting DNMT3B and DNMT1</article-title><source>Oncotarget</source><year>2015</year><volume>6</volume><fpage>38139</fpage><lpage>38150</lpage><pub-id pub-id-type="doi">10.18632/oncotarget.5709</pub-id><pub-id pub-id-type="pmid">26497367</pub-id></element-citation></ref><ref id="B111-cancers-11-01802"><label>111.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wang</surname><given-names>X.X.</given-names></name><name><surname>Guo</surname><given-names>G.C.</given-names></name><name><surname>Qian</surname><given-names>X.K.</given-names></name><name><surname>Dou</surname><given-names>D.W.</given-names></name><name><surname>Zhang</surname><given-names>Z.</given-names></name><name><surname>Xu</surname><given-names>X.D.</given-names></name><name><surname>Duan</surname><given-names>X.</given-names></name><name><surname>Pei</surname><given-names>X.H.</given-names></name></person-group><article-title>miR-506 attenuates methylation of lncRNA MEG3 to inhibit migration and invasion of breast cancer cell lines via targeting SP1 and SP3</article-title><source>Cancer Cell Int.</source><year>2018</year><volume>18</volume><fpage>171</fpage><pub-id pub-id-type="doi">10.1186/s12935-018-0642-8</pub-id><pub-id pub-id-type="pmid">30386180</pub-id></element-citation></ref><ref id="B112-cancers-11-01802"><label>112.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wen</surname><given-names>S.Y.</given-names></name><name><surname>Lin</surname><given-names>Y.</given-names></name><name><surname>Yu</surname><given-names>Y.Q.</given-names></name><name><surname>Cao</surname><given-names>S.J.</given-names></name><name><surname>Zhang</surname><given-names>R.</given-names></name><name><surname>Yang</surname><given-names>X.M.</given-names></name><name><surname>Li</surname><given-names>J.</given-names></name><name><surname>Zhang</surname><given-names>Y.L.</given-names></name><name><surname>Wang</surname><given-names>Y.H.</given-names></name><name><surname>Ma</surname><given-names>M.Z.</given-names></name><etal></etal></person-group><article-title>miR-506 acts as a tumor suppressor by directly targeting the hedgehog pathway transcription factor Gli3 in human cervical cancer</article-title><source>Oncogene</source><year>2015</year><volume>34</volume><fpage>717</fpage><lpage>725</lpage><pub-id pub-id-type="doi">10.1038/onc.2014.9</pub-id><pub-id pub-id-type="pmid">24608427</pub-id></element-citation></ref><ref id="B113-cancers-11-01802"><label>113.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Peng</surname><given-names>T.</given-names></name><name><surname>Zhou</surname><given-names>L.</given-names></name><name><surname>Zuo</surname><given-names>L.</given-names></name><name><surname>Luan</surname><given-names>Y.</given-names></name></person-group><article-title>MiR-506 functions as a tumor suppressor in glioma by targeting STAT3</article-title><source>Oncol. Rep.</source><year>2016</year><volume>35</volume><fpage>1057</fpage><lpage>1064</lpage><pub-id pub-id-type="doi">10.3892/or.2015.4406</pub-id><pub-id pub-id-type="pmid">26554866</pub-id></element-citation></ref><ref id="B114-cancers-11-01802"><label>114.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>J.</given-names></name><name><surname>Bian</surname><given-names>E.B.</given-names></name><name><surname>He</surname><given-names>X.J.</given-names></name><name><surname>Ma</surname><given-names>C.C.</given-names></name><name><surname>Zong</surname><given-names>G.</given-names></name><name><surname>Wang</surname><given-names>H.L.</given-names></name><name><surname>Zhao</surname><given-names>B.</given-names></name></person-group><article-title>Epigenetic repression of long non-coding RNA MEG3 mediated by DNMT1 represses the p53 pathway in gliomas</article-title><source>Int. J. Oncol.</source><year>2016</year><volume>48</volume><fpage>723</fpage><lpage>733</lpage><pub-id pub-id-type="doi">10.3892/ijo.2015.3285</pub-id><pub-id pub-id-type="pmid">26676363</pub-id></element-citation></ref><ref id="B115-cancers-11-01802"><label>115.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jiang</surname><given-names>Y.</given-names></name><name><surname>Lin</surname><given-names>L.</given-names></name><name><surname>Zhong</surname><given-names>S.</given-names></name><name><surname>Cai</surname><given-names>Y.</given-names></name><name><surname>Zhang</surname><given-names>F.</given-names></name><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Miao</surname><given-names>R.</given-names></name><name><surname>Zhang</surname><given-names>B.</given-names></name><name><surname>Gao</surname><given-names>S.</given-names></name><name><surname>Hu</surname><given-names>X.</given-names></name></person-group><article-title>Overexpression of novel lncRNA NLIPMT inhibits metastasis by reducing phosphorylated glycogen synthase kinase 3beta in breast cancer</article-title><source>J. Cell. Physiol.</source><year>2018</year><pub-id pub-id-type="doi">10.1002/jcp.27738</pub-id></element-citation></ref><ref id="B116-cancers-11-01802"><label>116.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Armanious</surname><given-names>H.</given-names></name><name><surname>Deschenes</surname><given-names>J.</given-names></name><name><surname>Gelebart</surname><given-names>P.</given-names></name><name><surname>Ghosh</surname><given-names>S.</given-names></name><name><surname>Mackey</surname><given-names>J.</given-names></name><name><surname>Lai</surname><given-names>R.</given-names></name></person-group><article-title>Clinical and biological significance of GSK-3β inactivation in breast cancer-an immunohistochemical study</article-title><source>Hum. Pathol.</source><year>2010</year><volume>41</volume><fpage>1657</fpage><lpage>1663</lpage><pub-id pub-id-type="doi">10.1016/j.humpath.2010.04.015</pub-id><pub-id pub-id-type="pmid">20709358</pub-id></element-citation></ref><ref id="B117-cancers-11-01802"><label>117.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dembowy</surname><given-names>J.</given-names></name><name><surname>Adissu</surname><given-names>H.</given-names></name><name><surname>Liu</surname><given-names>J.</given-names></name><name><surname>Zacksenhaus</surname><given-names>E.</given-names></name><name><surname>Woodgett</surname><given-names>J.</given-names></name></person-group><article-title>Effect of glycogen synthase kinase-3 inactivation on mouse mammary gland development and oncogenesis</article-title><source>Oncogene</source><year>2015</year><volume>34</volume><fpage>3514</fpage><lpage>3526</lpage><pub-id pub-id-type="doi">10.1038/onc.2014.279</pub-id><pub-id pub-id-type="pmid">25195860</pub-id></element-citation></ref><ref id="B118-cancers-11-01802"><label>118.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Farago</surname><given-names>M.</given-names></name><name><surname>Dominguez</surname><given-names>I.</given-names></name><name><surname>Landesman-Bollag</surname><given-names>E.</given-names></name><name><surname>Xu</surname><given-names>X.</given-names></name><name><surname>Rosner</surname><given-names>A.</given-names></name><name><surname>Cardiff</surname><given-names>R.</given-names></name><name><surname>Seldin</surname><given-names>D.</given-names></name></person-group><article-title>Kinase-inactive glycogen synthase kinase 3beta promotes Wnt signaling and mammary tumorigenesis</article-title><source>Cancer Res.</source><year>2005</year><volume>65</volume><fpage>5792</fpage><lpage>5801</lpage><pub-id pub-id-type="doi">10.1158/0008-5472.CAN-05-1021</pub-id><pub-id pub-id-type="pmid">15994955</pub-id></element-citation></ref><ref id="B119-cancers-11-01802"><label>119.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shakoori</surname><given-names>A.</given-names></name><name><surname>Mai</surname><given-names>W.</given-names></name><name><surname>Miyashita</surname><given-names>K.</given-names></name><name><surname>Yasumoto</surname><given-names>K.</given-names></name><name><surname>Takahashi</surname><given-names>Y.</given-names></name><name><surname>Ooi</surname><given-names>A.</given-names></name><name><surname>Kawakami</surname><given-names>K.</given-names></name><name><surname>Minamoto</surname><given-names>T.</given-names></name></person-group><article-title>Inhibition of GSK-3 beta activity attenuates proliferation of human colon cancer cells in rodents</article-title><source>Cancer Sci.</source><year>2007</year><volume>98</volume><fpage>1388</fpage><lpage>1393</lpage><pub-id pub-id-type="doi">10.1111/j.1349-7006.2007.00545.x</pub-id><pub-id pub-id-type="pmid">17640304</pub-id></element-citation></ref><ref id="B120-cancers-11-01802"><label>120.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bilim</surname><given-names>V.</given-names></name><name><surname>Ougolkov</surname><given-names>A.</given-names></name><name><surname>Yuuki</surname><given-names>K.</given-names></name><name><surname>Naito</surname><given-names>S.</given-names></name><name><surname>Kawazoe</surname><given-names>H.</given-names></name><name><surname>Muto</surname><given-names>A.</given-names></name><name><surname>Oya</surname><given-names>M.</given-names></name><name><surname>Billadeau</surname><given-names>D.</given-names></name><name><surname>Motoyama</surname><given-names>T.</given-names></name><name><surname>Tomita</surname><given-names>Y.</given-names></name></person-group><article-title>Glycogen synthase kinase-3: A new therapeutic target in renal cell carcinoma</article-title><source>Br. J. Cancer</source><year>2009</year><volume>101</volume><fpage>2005</fpage><lpage>2014</lpage><pub-id pub-id-type="doi">10.1038/sj.bjc.6605437</pub-id><pub-id pub-id-type="pmid">19920820</pub-id></element-citation></ref><ref id="B121-cancers-11-01802"><label>121.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xu</surname><given-names>R.</given-names></name><name><surname>Zhu</surname><given-names>X.</given-names></name><name><surname>Chen</surname><given-names>F.</given-names></name><name><surname>Huang</surname><given-names>C.</given-names></name><name><surname>Ai</surname><given-names>K.</given-names></name><name><surname>Wu</surname><given-names>H.</given-names></name><name><surname>Zhang</surname><given-names>L.</given-names></name><name><surname>Zhao</surname><given-names>X.</given-names></name></person-group><article-title>LncRNA XIST/miR-200c regulates the stemness properties and tumourigenicity of human bladder cancer stem cell-like cells</article-title><source>Cancer Cell Int.</source><year>2018</year><volume>18</volume><fpage>41</fpage><pub-id pub-id-type="doi">10.1186/s12935-018-0540-0</pub-id><pub-id pub-id-type="pmid">29559853</pub-id></element-citation></ref><ref id="B122-cancers-11-01802"><label>122.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tang</surname><given-names>Y.</given-names></name><name><surname>He</surname><given-names>R.</given-names></name><name><surname>An</surname><given-names>J.</given-names></name><name><surname>Deng</surname><given-names>P.</given-names></name><name><surname>Huang</surname><given-names>L.</given-names></name><name><surname>Yang</surname><given-names>W.</given-names></name></person-group><article-title>lncRNA XIST interacts with miR-140 to modulate lung cancer growth by targeting iASPP</article-title><source>Oncol. Rep.</source><year>2017</year><volume>38</volume><fpage>941</fpage><lpage>948</lpage><pub-id pub-id-type="doi">10.3892/or.2017.5751</pub-id><pub-id pub-id-type="pmid">28656261</pub-id></element-citation></ref><ref id="B123-cancers-11-01802"><label>123.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zheng</surname><given-names>R.</given-names></name><name><surname>Lin</surname><given-names>S.</given-names></name><name><surname>Guan</surname><given-names>L.</given-names></name><name><surname>Yuan</surname><given-names>H.</given-names></name><name><surname>Liu</surname><given-names>K.</given-names></name><name><surname>Liu</surname><given-names>C.</given-names></name><name><surname>Ye</surname><given-names>W.</given-names></name><name><surname>Liao</surname><given-names>Y.</given-names></name><name><surname>Jia</surname><given-names>J.</given-names></name><name><surname>Zhang</surname><given-names>R.</given-names></name></person-group><article-title>Long non-coding RNA XIST inhibited breast cancer cell growth, migration, and invasion via miR-155/CDX1 axis</article-title><source>Biochem. Biophys. Res. Commun.</source><year>2018</year><volume>498</volume><fpage>1002</fpage><lpage>1008</lpage><pub-id pub-id-type="doi">10.1016/j.bbrc.2018.03.104</pub-id><pub-id pub-id-type="pmid">29550489</pub-id></element-citation></ref><ref id="B124-cancers-11-01802"><label>124.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hashimoto</surname><given-names>S.</given-names></name><name><surname>Amaya</surname><given-names>F.</given-names></name><name><surname>Matsuyama</surname><given-names>H.</given-names></name><name><surname>Ueno</surname><given-names>H.</given-names></name><name><surname>Kikuchi</surname><given-names>S.</given-names></name><name><surname>Tanaka</surname><given-names>M.</given-names></name><name><surname>Watanabe</surname><given-names>Y.</given-names></name><name><surname>Ebina</surname><given-names>M.</given-names></name><name><surname>Ishizaka</surname><given-names>A.</given-names></name><name><surname>Tsukita</surname><given-names>S.</given-names></name><etal></etal></person-group><article-title>Dysregulation of lung injury and repair in moesin-deficient mice treated with intratracheal bleomycin</article-title><source>Am. J. Physiol. Lung Cell. Mol. Physiol.</source><year>2008</year><volume>295</volume><fpage>L566</fpage><lpage>L574</lpage><pub-id pub-id-type="doi">10.1152/ajplung.90250.2008</pub-id><pub-id pub-id-type="pmid">18658275</pub-id></element-citation></ref><ref id="B125-cancers-11-01802"><label>125.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xing</surname><given-names>F.</given-names></name><name><surname>Liu</surname><given-names>Y.</given-names></name><name><surname>Wu</surname><given-names>S.Y.</given-names></name><name><surname>Wu</surname><given-names>K.</given-names></name><name><surname>Sharma</surname><given-names>S.</given-names></name><name><surname>Mo</surname><given-names>Y.Y.</given-names></name><name><surname>Feng</surname><given-names>J.</given-names></name><name><surname>Sanders</surname><given-names>S.</given-names></name><name><surname>Jin</surname><given-names>G.</given-names></name><name><surname>Singh</surname><given-names>R.</given-names></name><etal></etal></person-group><article-title>Loss of XIST in Breast Cancer Activates MSN-c-Met and Reprograms Microglia via Exosomal miRNA to Promote Brain Metastasis</article-title><source>Cancer Res.</source><year>2018</year><volume>78</volume><fpage>4316</fpage><lpage>4330</lpage><pub-id pub-id-type="doi">10.1158/0008-5472.CAN-18-1102</pub-id><pub-id pub-id-type="pmid">30026327</pub-id></element-citation></ref><ref id="B126-cancers-11-01802"><label>126.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Salter</surname><given-names>M.W.</given-names></name><name><surname>Stevens</surname><given-names>B.</given-names></name></person-group><article-title>Microglia emerge as central players in brain disease</article-title><source>Nat. Med.</source><year>2017</year><volume>23</volume><fpage>1018</fpage><lpage>1027</lpage><pub-id pub-id-type="doi">10.1038/nm.4397</pub-id><pub-id pub-id-type="pmid">28886007</pub-id></element-citation></ref><ref id="B127-cancers-11-01802"><label>127.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Reya</surname><given-names>T.</given-names></name><name><surname>Morrison</surname><given-names>S.J.</given-names></name><name><surname>Clarke</surname><given-names>M.F.</given-names></name><name><surname>Weissman</surname><given-names>I.L.</given-names></name></person-group><article-title>Stem cells, cancer, and cancer stem cells</article-title><source>Nature</source><year>2001</year><volume>414</volume><fpage>105</fpage><lpage>111</lpage><pub-id pub-id-type="doi">10.1038/35102167</pub-id><pub-id pub-id-type="pmid">11689955</pub-id></element-citation></ref><ref id="B128-cancers-11-01802"><label>128.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Adorno-Cruz</surname><given-names>V.</given-names></name><name><surname>Kibria</surname><given-names>G.</given-names></name><name><surname>Liu</surname><given-names>X.</given-names></name><name><surname>Doherty</surname><given-names>M.</given-names></name><name><surname>Junk</surname><given-names>D.J.</given-names></name><name><surname>Guan</surname><given-names>D.</given-names></name><name><surname>Hubert</surname><given-names>C.</given-names></name><name><surname>Venere</surname><given-names>M.</given-names></name><name><surname>Mulkearns-Hubert</surname><given-names>E.</given-names></name><name><surname>Sinyuk</surname><given-names>M.</given-names></name><etal></etal></person-group><article-title>Cancer stem cells: Targeting the roots of cancer, seeds of metastasis, and sources of therapy resistance</article-title><source>Cancer Res.</source><year>2015</year><volume>75</volume><fpage>924</fpage><lpage>929</lpage><pub-id pub-id-type="doi">10.1158/0008-5472.CAN-14-3225</pub-id><pub-id pub-id-type="pmid">25604264</pub-id></element-citation></ref><ref id="B129-cancers-11-01802"><label>129.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Baccelli</surname><given-names>I.</given-names></name><name><surname>Trumpp</surname><given-names>A.</given-names></name></person-group><article-title>The evolving concept of cancer and metastasis stem cells</article-title><source>J. Cell Biol.</source><year>2012</year><volume>198</volume><fpage>281</fpage><lpage>293</lpage><pub-id pub-id-type="doi">10.1083/jcb.201202014</pub-id><pub-id pub-id-type="pmid">22869594</pub-id></element-citation></ref><ref id="B130-cancers-11-01802"><label>130.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Antoniou</surname><given-names>A.</given-names></name><name><surname>Hebrant</surname><given-names>A.</given-names></name><name><surname>Dom</surname><given-names>G.</given-names></name><name><surname>Dumont</surname><given-names>J.E.</given-names></name><name><surname>Maenhaut</surname><given-names>C.</given-names></name></person-group><article-title>Cancer stem cells, a fuzzy evolving concept: A cell population or a cell property?</article-title><source>Cell Cycle</source><year>2013</year><volume>12</volume><fpage>3743</fpage><lpage>3748</lpage><pub-id pub-id-type="doi">10.4161/cc.27305</pub-id><pub-id pub-id-type="pmid">24270846</pub-id></element-citation></ref><ref id="B131-cancers-11-01802"><label>131.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Castro-Oropeza</surname><given-names>R.</given-names></name><name><surname>Melendez-Zajgla</surname><given-names>J.</given-names></name><name><surname>Maldonado</surname><given-names>V.</given-names></name><name><surname>Vazquez-Santillan</surname><given-names>K.</given-names></name></person-group><article-title>The emerging role of lncRNAs in the regulation of cancer stem cells</article-title><source>Cell. Oncol.</source><year>2018</year><volume>41</volume><fpage>585</fpage><lpage>603</lpage><pub-id pub-id-type="doi">10.1007/s13402-018-0406-4</pub-id></element-citation></ref><ref id="B132-cancers-11-01802"><label>132.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mani</surname><given-names>S.</given-names></name><name><surname>Guo</surname><given-names>W.</given-names></name><name><surname>Liao</surname><given-names>M.</given-names></name><name><surname>Eaton</surname><given-names>E.</given-names></name><name><surname>Ayyanan</surname><given-names>A.</given-names></name><name><surname>Zhou</surname><given-names>A.</given-names></name><name><surname>Brooks</surname><given-names>M.</given-names></name><name><surname>Reinhard</surname><given-names>F.</given-names></name><name><surname>Zhang</surname><given-names>C.</given-names></name><name><surname>Shipitsin</surname><given-names>M.</given-names></name><etal></etal></person-group><article-title>The epithelial-mesenchymal transition generates cells with properties of stem cells</article-title><source>Cell</source><year>2008</year><volume>133</volume><fpage>704</fpage><lpage>715</lpage><pub-id pub-id-type="doi">10.1016/j.cell.2008.03.027</pub-id><pub-id pub-id-type="pmid">18485877</pub-id></element-citation></ref><ref id="B133-cancers-11-01802"><label>133.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hardin</surname><given-names>H.</given-names></name><name><surname>Zhang</surname><given-names>R.</given-names></name><name><surname>Helein</surname><given-names>H.</given-names></name><name><surname>Buehler</surname><given-names>D.</given-names></name><name><surname>Guo</surname><given-names>Z.</given-names></name><name><surname>Lloyd</surname><given-names>R.V.</given-names></name></person-group><article-title>The evolving concept of cancer stem-like cells in thyroid cancer and other solid tumors</article-title><source>Lab. Investig.</source><year>2017</year><volume>97</volume><fpage>1142</fpage><lpage>1151</lpage><pub-id pub-id-type="doi">10.1038/labinvest.2017.41</pub-id><pub-id pub-id-type="pmid">28394318</pub-id></element-citation></ref><ref id="B134-cancers-11-01802"><label>134.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>H.</given-names></name><name><surname>Zhu</surname><given-names>L.</given-names></name><name><surname>Xu</surname><given-names>L.</given-names></name><name><surname>Qin</surname><given-names>K.</given-names></name><name><surname>Liu</surname><given-names>C.</given-names></name><name><surname>Yu</surname><given-names>Y.</given-names></name><name><surname>Su</surname><given-names>D.</given-names></name><name><surname>Wu</surname><given-names>K.</given-names></name><name><surname>Sheng</surname><given-names>Y.</given-names></name></person-group><article-title>Long noncoding RNA linc00617 exhibits oncogenic activity in breast cancer</article-title><source>Mol. Carcinog.</source><year>2017</year><volume>56</volume><fpage>3</fpage><lpage>17</lpage><pub-id pub-id-type="doi">10.1002/mc.22338</pub-id><pub-id pub-id-type="pmid">26207516</pub-id></element-citation></ref><ref id="B135-cancers-11-01802"><label>135.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Keshavarz</surname><given-names>M.</given-names></name><name><surname>Asadi</surname><given-names>M.H.</given-names></name></person-group><article-title>Long non-coding RNA ES1 controls the proliferation of breast cancer cells by regulating the Oct4/Sox2/miR-302 axis</article-title><source>FEBS J.</source><year>2019</year><volume>286</volume><fpage>2611</fpage><lpage>2623</lpage><pub-id pub-id-type="doi">10.1111/febs.14825</pub-id><pub-id pub-id-type="pmid">30927330</pub-id></element-citation></ref><ref id="B136-cancers-11-01802"><label>136.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhou</surname><given-names>M.</given-names></name><name><surname>Hou</surname><given-names>Y.</given-names></name><name><surname>Yang</surname><given-names>G.</given-names></name><name><surname>Zhang</surname><given-names>H.</given-names></name><name><surname>Tu</surname><given-names>G.</given-names></name><name><surname>Du</surname><given-names>Y.E.</given-names></name><name><surname>Wen</surname><given-names>S.</given-names></name><name><surname>Xu</surname><given-names>L.</given-names></name><name><surname>Tang</surname><given-names>X.</given-names></name><name><surname>Tang</surname><given-names>S.</given-names></name><etal></etal></person-group><article-title>LncRNA-Hh Strengthen Cancer Stem Cells Generation in Twist-Positive Breast Cancer via Activation of Hedgehog Signaling Pathway</article-title><source>Stem Cells</source><year>2016</year><volume>34</volume><fpage>55</fpage><lpage>66</lpage><pub-id pub-id-type="doi">10.1002/stem.2219</pub-id><pub-id pub-id-type="pmid">26418365</pub-id></element-citation></ref><ref id="B137-cancers-11-01802"><label>137.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Deng</surname><given-names>J.</given-names></name><name><surname>Yang</surname><given-names>M.</given-names></name><name><surname>Jiang</surname><given-names>R.</given-names></name><name><surname>An</surname><given-names>N.</given-names></name><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Liu</surname><given-names>B.</given-names></name></person-group><article-title>Long Non-Coding RNA HOTAIR Regulates the Proliferation, Self-Renewal Capacity, Tumor Formation and Migration of the Cancer Stem-Like Cell (CSC) Subpopulation Enriched from Breast Cancer Cells</article-title><source>PLoS ONE</source><year>2017</year><volume>12</volume><elocation-id>e0170860</elocation-id><pub-id pub-id-type="doi">10.1371/journal.pone.0170860</pub-id><pub-id pub-id-type="pmid">28122024</pub-id></element-citation></ref><ref id="B138-cancers-11-01802"><label>138.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>Z.</given-names></name><name><surname>Sun</surname><given-names>L.</given-names></name><name><surname>Zhang</surname><given-names>Y.</given-names></name><name><surname>Lu</surname><given-names>G.</given-names></name><name><surname>Li</surname><given-names>Y.</given-names></name><name><surname>Wei</surname><given-names>Z.</given-names></name></person-group><article-title>Long non-coding RNA FEZF1-AS1 promotes breast cancer stemness and tumorigenesis via targeting miR-30a/Nanog axis</article-title><source>J. Cell. Physiol.</source><year>2018</year><volume>233</volume><fpage>8630</fpage><lpage>8638</lpage><pub-id pub-id-type="doi">10.1002/jcp.26611</pub-id><pub-id pub-id-type="pmid">29797562</pub-id></element-citation></ref><ref id="B139-cancers-11-01802"><label>139.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lu</surname><given-names>G.</given-names></name><name><surname>Li</surname><given-names>Y.</given-names></name><name><surname>Ma</surname><given-names>Y.</given-names></name><name><surname>Lu</surname><given-names>J.</given-names></name><name><surname>Chen</surname><given-names>Y.</given-names></name><name><surname>Jiang</surname><given-names>Q.</given-names></name><name><surname>Qin</surname><given-names>Q.</given-names></name><name><surname>Zhao</surname><given-names>L.</given-names></name><name><surname>Huang</surname><given-names>Q.</given-names></name><name><surname>Luo</surname><given-names>Z.</given-names></name><etal></etal></person-group><article-title>Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p/E2F1/Nanog axis</article-title><source>J. Exp. Clin. Cancer Res.</source><year>2018</year><volume>37</volume><fpage>289</fpage><pub-id pub-id-type="doi">10.1186/s13046-018-0945-6</pub-id><pub-id pub-id-type="pmid">30482236</pub-id></element-citation></ref><ref id="B140-cancers-11-01802"><label>140.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Huang</surname><given-names>H.</given-names></name><name><surname>Weng</surname><given-names>H.</given-names></name><name><surname>Sun</surname><given-names>W.</given-names></name><name><surname>Qin</surname><given-names>X.</given-names></name><name><surname>Shi</surname><given-names>H.</given-names></name><name><surname>Wu</surname><given-names>H.</given-names></name><name><surname>Zhao</surname><given-names>B.S.</given-names></name><name><surname>Mesquita</surname><given-names>A.</given-names></name><name><surname>Liu</surname><given-names>C.</given-names></name><name><surname>Yuan</surname><given-names>C.L.</given-names></name><etal></etal></person-group><article-title>Recognition of RNA N(6)-methyladenosine by IGF2BP proteins enhances mRNA stability and translation</article-title><source>Nat. Cell Biol.</source><year>2018</year><volume>20</volume><fpage>285</fpage><lpage>295</lpage><pub-id pub-id-type="doi">10.1038/s41556-018-0045-z</pub-id><pub-id pub-id-type="pmid">29476152</pub-id></element-citation></ref><ref id="B141-cancers-11-01802"><label>141.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ma</surname><given-names>F.</given-names></name><name><surname>Liu</surname><given-names>X.</given-names></name><name><surname>Zhou</surname><given-names>S.</given-names></name><name><surname>Li</surname><given-names>W.</given-names></name><name><surname>Liu</surname><given-names>C.</given-names></name><name><surname>Chadwick</surname><given-names>M.</given-names></name><name><surname>Qian</surname><given-names>C.</given-names></name></person-group><article-title>Long non-coding RNA FGF13-AS1 inhibits glycolysis and stemness properties of breast cancer cells through FGF13-AS1/IGF2BPs/Myc feedback loop</article-title><source>Cancer Lett.</source><year>2019</year><volume>450</volume><fpage>63</fpage><lpage>75</lpage><pub-id pub-id-type="doi">10.1016/j.canlet.2019.02.008</pub-id><pub-id pub-id-type="pmid">30771425</pub-id></element-citation></ref><ref id="B142-cancers-11-01802"><label>142.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>S.</given-names></name><name><surname>Hu</surname><given-names>X.</given-names></name><name><surname>Zhang</surname><given-names>W.</given-names></name><name><surname>Tam</surname><given-names>K.</given-names></name></person-group><article-title>Unexpected Discovery of Dichloroacetate Derived Adenosine Triphosphate Competitors Targeting Pyruvate Dehydrogenase Kinase To Inhibit Cancer Proliferation</article-title><source>J. Med. Chem.</source><year>2016</year><volume>59</volume><fpage>3562</fpage><lpage>3568</lpage><pub-id pub-id-type="doi">10.1021/acs.jmedchem.5b01828</pub-id><pub-id pub-id-type="pmid">27006991</pub-id></element-citation></ref><ref id="B143-cancers-11-01802"><label>143.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Peng</surname><given-names>F.</given-names></name><name><surname>Wang</surname><given-names>J.H.</given-names></name><name><surname>Fan</surname><given-names>W.J.</given-names></name><name><surname>Meng</surname><given-names>Y.T.</given-names></name><name><surname>Li</surname><given-names>M.M.</given-names></name><name><surname>Li</surname><given-names>T.T.</given-names></name><name><surname>Cui</surname><given-names>B.</given-names></name><name><surname>Wang</surname><given-names>H.F.</given-names></name><name><surname>Zhao</surname><given-names>Y.</given-names></name><name><surname>An</surname><given-names>F.</given-names></name><etal></etal></person-group><article-title>Glycolysis gatekeeper PDK1 reprograms breast cancer stem cells under hypoxia</article-title><source>Oncogene</source><year>2018</year><volume>37</volume><fpage>1062</fpage><lpage>1074</lpage><pub-id pub-id-type="doi">10.1038/onc.2017.368</pub-id><pub-id pub-id-type="pmid">29106390</pub-id></element-citation></ref><ref id="B144-cancers-11-01802"><label>144.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dupuy</surname><given-names>F.</given-names></name><name><surname>Tabariès</surname><given-names>S.</given-names></name><name><surname>Andrzejewski</surname><given-names>S.</given-names></name><name><surname>Dong</surname><given-names>Z.</given-names></name><name><surname>Blagih</surname><given-names>J.</given-names></name><name><surname>Annis</surname><given-names>M.</given-names></name><name><surname>Omeroglu</surname><given-names>A.</given-names></name><name><surname>Gao</surname><given-names>D.</given-names></name><name><surname>Leung</surname><given-names>S.</given-names></name><name><surname>Amir</surname><given-names>E.</given-names></name><etal></etal></person-group><article-title>PDK1-Dependent Metabolic Reprogramming Dictates Metastatic Potential in Breast Cancer</article-title><source>Cell Metab.</source><year>2015</year><volume>22</volume><fpage>577</fpage><lpage>589</lpage><pub-id pub-id-type="doi">10.1016/j.cmet.2015.08.007</pub-id><pub-id pub-id-type="pmid">26365179</pub-id></element-citation></ref><ref id="B145-cancers-11-01802"><label>145.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Velpula</surname><given-names>K.</given-names></name><name><surname>Bhasin</surname><given-names>A.</given-names></name><name><surname>Asuthkar</surname><given-names>S.</given-names></name><name><surname>Tsung</surname><given-names>A.</given-names></name></person-group><article-title>Combined targeting of PDK1 and EGFR triggers regression of glioblastoma by reversing the Warburg effect</article-title><source>Cancer Res.</source><year>2013</year><volume>73</volume><fpage>7277</fpage><lpage>7289</lpage><pub-id pub-id-type="doi">10.1158/0008-5472.CAN-13-1868</pub-id><pub-id pub-id-type="pmid">24148623</pub-id></element-citation></ref><ref id="B146-cancers-11-01802"><label>146.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>C.</given-names></name><name><surname>Shan</surname><given-names>S.</given-names></name><name><surname>Huang</surname><given-names>Q.</given-names></name><name><surname>Braun</surname><given-names>R.</given-names></name><name><surname>Lanzen</surname><given-names>J.</given-names></name><name><surname>Hu</surname><given-names>K.</given-names></name><name><surname>Lin</surname><given-names>P.</given-names></name><name><surname>Dewhirst</surname><given-names>M.</given-names></name></person-group><article-title>Initial stages of tumor cell-induced angiogenesis: Evaluation via skin window chambers in rodent models</article-title><source>J. Natl. Cancer Inst.</source><year>2000</year><volume>92</volume><fpage>143</fpage><lpage>147</lpage><pub-id pub-id-type="doi">10.1093/jnci/92.2.143</pub-id><pub-id pub-id-type="pmid">10639516</pub-id></element-citation></ref><ref id="B147-cancers-11-01802"><label>147.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Johnson</surname><given-names>K.E.</given-names></name><name><surname>Wilgus</surname><given-names>T.A.</given-names></name></person-group><article-title>Vascular Endothelial Growth Factor and Angiogenesis in the Regulation of Cutaneous Wound Repair</article-title><source>Adv. Wound Care</source><year>2014</year><volume>3</volume><fpage>647</fpage><lpage>661</lpage><pub-id pub-id-type="doi">10.1089/wound.2013.0517</pub-id><pub-id pub-id-type="pmid">25302139</pub-id></element-citation></ref><ref id="B148-cancers-11-01802"><label>148.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Huang</surname><given-names>X.J.</given-names></name><name><surname>Xia</surname><given-names>Y.</given-names></name><name><surname>He</surname><given-names>G.F.</given-names></name><name><surname>Zheng</surname><given-names>L.L.</given-names></name><name><surname>Cai</surname><given-names>Y.P.</given-names></name><name><surname>Yin</surname><given-names>Y.</given-names></name><name><surname>Wu</surname><given-names>Q.</given-names></name></person-group><article-title>MALAT1 promotes angiogenesis of breast cancer</article-title><source>Oncol. Rep.</source><year>2018</year><volume>40</volume><fpage>2683</fpage><lpage>2689</lpage><pub-id pub-id-type="doi">10.3892/or.2018.6705</pub-id><pub-id pub-id-type="pmid">30226550</pub-id></element-citation></ref><ref id="B149-cancers-11-01802"><label>149.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Al-Rugeebah</surname><given-names>A.</given-names></name><name><surname>Alanazi</surname><given-names>M.</given-names></name><name><surname>Parine</surname><given-names>N.R.</given-names></name></person-group><article-title>MEG3: An Oncogenic Long Non-coding RNA in Different Cancers</article-title><source>Pathol. Oncol. Res.</source><year>2019</year><volume>25</volume><fpage>859</fpage><lpage>874</lpage><pub-id pub-id-type="doi">10.1007/s12253-019-00614-3</pub-id><pub-id pub-id-type="pmid">30793226</pub-id></element-citation></ref><ref id="B150-cancers-11-01802"><label>150.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>C.Y.</given-names></name><name><surname>Yu</surname><given-names>M.S.</given-names></name><name><surname>Li</surname><given-names>X.</given-names></name><name><surname>Zhang</surname><given-names>Z.</given-names></name><name><surname>Han</surname><given-names>C.R.</given-names></name><name><surname>Yan</surname><given-names>B.</given-names></name></person-group><article-title>Overexpression of long non-coding RNA MEG3 suppresses breast cancer cell proliferation, invasion, and angiogenesis through AKT pathway</article-title><source>Tumour Biol.</source><year>2017</year><volume>39</volume><pub-id pub-id-type="doi">10.1177/1010428317701311</pub-id></element-citation></ref><ref id="B151-cancers-11-01802"><label>151.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Senkus</surname><given-names>E.</given-names></name><name><surname>Kyriakides</surname><given-names>S.</given-names></name><name><surname>Ohno</surname><given-names>S.</given-names></name><name><surname>Penault-Llorca</surname><given-names>F.</given-names></name><name><surname>Poortmans</surname><given-names>P.</given-names></name><name><surname>Rutgers</surname><given-names>E.</given-names></name><name><surname>Zackrisson</surname><given-names>S.</given-names></name><name><surname>Cardoso</surname><given-names>F.</given-names></name></person-group><article-title>Primary breast cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up</article-title><source>Ann. Oncol.</source><year>2015</year><volume>26</volume><issue>Suppl. 5</issue><fpage>v8</fpage><lpage>v30</lpage><pub-id pub-id-type="doi">10.1093/annonc/mdv298</pub-id><pub-id pub-id-type="pmid">26314782</pub-id></element-citation></ref><ref id="B152-cancers-11-01802"><label>152.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Slamon</surname><given-names>D.</given-names></name><name><surname>Neven</surname><given-names>P.</given-names></name><name><surname>Chia</surname><given-names>S.</given-names></name><name><surname>Fasching</surname><given-names>P.</given-names></name><name><surname>De Laurentiis</surname><given-names>M.</given-names></name><name><surname>Im</surname><given-names>S.</given-names></name><name><surname>Petrakova</surname><given-names>K.</given-names></name><name><surname>Bianchi</surname><given-names>G.</given-names></name><name><surname>Esteva</surname><given-names>F.</given-names></name><name><surname>Martín</surname><given-names>M.</given-names></name><etal></etal></person-group><article-title>Phase III Randomized Study of Ribociclib and Fulvestrant in Hormone Receptor-Positive, Human Epidermal Growth Factor Receptor 2-Negative Advanced Breast Cancer: MONALEESA-3</article-title><source>J. Clin. Oncol.</source><year>2018</year><volume>36</volume><fpage>2465</fpage><lpage>2472</lpage><pub-id pub-id-type="doi">10.1200/JCO.2018.78.9909</pub-id><pub-id pub-id-type="pmid">29860922</pub-id></element-citation></ref><ref id="B153-cancers-11-01802"><label>153.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Vogel</surname><given-names>C.</given-names></name><name><surname>Cobleigh</surname><given-names>M.</given-names></name><name><surname>Tripathy</surname><given-names>D.</given-names></name><name><surname>Gutheil</surname><given-names>J.</given-names></name><name><surname>Harris</surname><given-names>L.</given-names></name><name><surname>Fehrenbacher</surname><given-names>L.</given-names></name><name><surname>Slamon</surname><given-names>D.</given-names></name><name><surname>Murphy</surname><given-names>M.</given-names></name><name><surname>Novotny</surname><given-names>W.</given-names></name><name><surname>Burchmore</surname><given-names>M.</given-names></name><etal></etal></person-group><article-title>Efficacy and safety of trastuzumab as a single agent in first-line treatment of HER2-overexpressing metastatic breast cancer</article-title><source>J. Clin. Oncol.</source><year>2002</year><volume>20</volume><fpage>719</fpage><lpage>726</lpage><pub-id pub-id-type="doi">10.1200/JCO.2002.20.3.719</pub-id><pub-id pub-id-type="pmid">11821453</pub-id></element-citation></ref><ref id="B154-cancers-11-01802"><label>154.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Collins</surname><given-names>D.</given-names></name><name><surname>Conlon</surname><given-names>N.</given-names></name><name><surname>Kannan</surname><given-names>S.</given-names></name><name><surname>Verma</surname><given-names>C.</given-names></name><name><surname>Eli</surname><given-names>L.</given-names></name><name><surname>Lalani</surname><given-names>A.</given-names></name><name><surname>Crown</surname><given-names>J.</given-names></name></person-group><article-title>Preclinical Characteristics of the Irreversible Pan-HER Kinase Inhibitor Neratinib Compared with Lapatinib: Implications for the Treatment of HER2-Positive and -Mutated Breast Cancer</article-title><source>Cancers</source><year>2019</year><volume>11</volume><elocation-id>737</elocation-id><pub-id pub-id-type="doi">10.3390/cancers11060737</pub-id><pub-id pub-id-type="pmid">31141894</pub-id></element-citation></ref><ref id="B155-cancers-11-01802"><label>155.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kim</surname><given-names>S.</given-names></name><name><surname>Dent</surname><given-names>R.</given-names></name><name><surname>Im</surname><given-names>S.</given-names></name><name><surname>Espié</surname><given-names>M.</given-names></name><name><surname>Blau</surname><given-names>S.</given-names></name><name><surname>Tan</surname><given-names>A.</given-names></name><name><surname>Isakoff</surname><given-names>S.</given-names></name><name><surname>Oliveira</surname><given-names>M.</given-names></name><name><surname>Saura</surname><given-names>C.</given-names></name><name><surname>Wongchenko</surname><given-names>M.</given-names></name><etal></etal></person-group><article-title>Ipatasertib plus paclitaxel versus placebo plus paclitaxel as first-line therapy for metastatic triple-negative breast cancer (LOTUS): A multicentre, randomised, double-blind, placebo-controlled, phase 2 trial</article-title><source>Lancet Oncol.</source><year>2017</year><volume>18</volume><fpage>1360</fpage><lpage>1372</lpage><pub-id pub-id-type="doi">10.1016/S1470-2045(17)30450-3</pub-id><pub-id pub-id-type="pmid">28800861</pub-id></element-citation></ref><ref id="B156-cancers-11-01802"><label>156.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pan</surname><given-names>H.</given-names></name><name><surname>Gray</surname><given-names>R.</given-names></name><name><surname>Braybrooke</surname><given-names>J.</given-names></name><name><surname>Davies</surname><given-names>C.</given-names></name><name><surname>Taylor</surname><given-names>C.</given-names></name><name><surname>McGale</surname><given-names>P.</given-names></name><name><surname>Peto</surname><given-names>R.</given-names></name><name><surname>Pritchard</surname><given-names>K.</given-names></name><name><surname>Bergh</surname><given-names>J.</given-names></name><name><surname>Dowsett</surname><given-names>M.</given-names></name><etal></etal></person-group><article-title>20-Year Risks of Breast-Cancer Recurrence after Stopping Endocrine Therapy at 5 Years</article-title><source>N. Engl. J. Med.</source><year>2017</year><volume>377</volume><fpage>1836</fpage><lpage>1846</lpage><pub-id pub-id-type="doi">10.1056/NEJMoa1701830</pub-id><pub-id pub-id-type="pmid">29117498</pub-id></element-citation></ref><ref id="B157-cancers-11-01802"><label>157.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dong</surname><given-names>H.</given-names></name><name><surname>Hu</surname><given-names>J.</given-names></name><name><surname>Zou</surname><given-names>K.</given-names></name><name><surname>Ye</surname><given-names>M.</given-names></name><name><surname>Chen</surname><given-names>Y.</given-names></name><name><surname>Wu</surname><given-names>C.</given-names></name><name><surname>Chen</surname><given-names>X.</given-names></name><name><surname>Han</surname><given-names>M.</given-names></name></person-group><article-title>Activation of LncRNA TINCR by H3K27 acetylation promotes Trastuzumab resistance and epithelial-mesenchymal transition by targeting MicroRNA-125b in breast Cancer</article-title><source>Mol. Cancer</source><year>2019</year><volume>18</volume><fpage>3</fpage><pub-id pub-id-type="doi">10.1186/s12943-018-0931-9</pub-id><pub-id pub-id-type="pmid">30621694</pub-id></element-citation></ref><ref id="B158-cancers-11-01802"><label>158.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wu</surname><given-names>Y.</given-names></name><name><surname>Sarkissyan</surname><given-names>M.</given-names></name><name><surname>Vadgama</surname><given-names>J.V.</given-names></name></person-group><article-title>Epithelial-Mesenchymal Transition and Breast Cancer</article-title><source>J. Clin. Med.</source><year>2016</year><volume>5</volume><elocation-id>13</elocation-id><pub-id pub-id-type="doi">10.3390/jcm5020013</pub-id></element-citation></ref><ref id="B159-cancers-11-01802"><label>159.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>X.</given-names></name><name><surname>Wang</surname><given-names>S.</given-names></name><name><surname>Li</surname><given-names>Z.</given-names></name><name><surname>Long</surname><given-names>X.</given-names></name><name><surname>Guo</surname><given-names>Z.</given-names></name><name><surname>Zhang</surname><given-names>G.</given-names></name><name><surname>Zu</surname><given-names>J.</given-names></name><name><surname>Chen</surname><given-names>Y.</given-names></name><name><surname>Wen</surname><given-names>L.</given-names></name></person-group><article-title>Retracted: NEAT1 induces epithelial-mesenchymal transition and 5-FU resistance through the miR-129/ZEB2 axis in breast cancer</article-title><source>FEBS Lett.</source><year>2016</year><pub-id pub-id-type="doi">10.1002/1873-3468.12474</pub-id></element-citation></ref><ref id="B160-cancers-11-01802"><label>160.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>X.</given-names></name><name><surname>Wang</surname><given-names>S.</given-names></name><name><surname>Li</surname><given-names>Z.</given-names></name><name><surname>Long</surname><given-names>X.</given-names></name><name><surname>Guo</surname><given-names>Z.</given-names></name><name><surname>Zhang</surname><given-names>G.</given-names></name><name><surname>Zu</surname><given-names>J.</given-names></name><name><surname>Chen</surname><given-names>Y.</given-names></name><name><surname>Wen</surname><given-names>L.</given-names></name></person-group><article-title>The lncRNA NEAT1 facilitates cell growth and invasion via the miR-211/HMGA2 axis in breast cancer</article-title><source>Int. J. Biol. Macromol.</source><year>2017</year><volume>105</volume><fpage>346</fpage><lpage>353</lpage><pub-id pub-id-type="doi">10.1016/j.ijbiomac.2017.07.053</pub-id><pub-id pub-id-type="pmid">28720546</pub-id></element-citation></ref><ref id="B161-cancers-11-01802"><label>161.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hu</surname><given-names>X.</given-names></name><name><surname>Hou</surname><given-names>P.</given-names></name><name><surname>Li</surname><given-names>T.</given-names></name><name><surname>Quan</surname><given-names>H.</given-names></name><name><surname>Li</surname><given-names>M.</given-names></name><name><surname>Lin</surname><given-names>T.</given-names></name><name><surname>Liu</surname><given-names>J.</given-names></name><name><surname>Bai</surname><given-names>J.</given-names></name><name><surname>Zheng</surname><given-names>J.</given-names></name></person-group><article-title>The roles of Wnt/β-catenin signaling pathway related lncRNAs in cancer</article-title><source>Int. J. Biol. Sci.</source><year>2018</year><volume>14</volume><fpage>2003</fpage><lpage>2011</lpage><pub-id pub-id-type="doi">10.7150/ijbs.27977</pub-id><pub-id pub-id-type="pmid">30585264</pub-id></element-citation></ref><ref id="B162-cancers-11-01802"><label>162.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sun</surname><given-names>X.</given-names></name><name><surname>Huang</surname><given-names>T.</given-names></name><name><surname>Zhang</surname><given-names>C.</given-names></name><name><surname>Zhang</surname><given-names>S.</given-names></name><name><surname>Wang</surname><given-names>Y.</given-names></name><name><surname>Zhang</surname><given-names>Q.</given-names></name><name><surname>Liu</surname><given-names>Z.</given-names></name></person-group><article-title>Long non-coding RNA LINC00968 reduces cell proliferation and migration and angiogenesis in breast cancer through up-regulation of PROX1 by reducing hsa-miR-423-5p</article-title><source>Cell Cycle</source><year>2019</year><volume>18</volume><fpage>1908</fpage><lpage>1924</lpage><pub-id pub-id-type="doi">10.1080/15384101.2019.1632641</pub-id><pub-id pub-id-type="pmid">31213129</pub-id></element-citation></ref><ref id="B163-cancers-11-01802"><label>163.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xiu</surname><given-names>D.</given-names></name><name><surname>Liu</surname><given-names>G.</given-names></name><name><surname>Yu</surname><given-names>S.</given-names></name><name><surname>Li</surname><given-names>L.</given-names></name><name><surname>Zhao</surname><given-names>G.</given-names></name><name><surname>Liu</surname><given-names>L.</given-names></name><name><surname>Li</surname><given-names>X.</given-names></name></person-group><article-title>Long non-coding RNA LINC00968 attenuates drug resistance of breast cancer cells through inhibiting the Wnt2/β-catenin signaling pathway by regulating WNT2</article-title><source>J. Exp. Clin. Cancer Res. CR</source><year>2019</year><volume>38</volume><fpage>94</fpage><pub-id pub-id-type="doi">10.1186/s13046-019-1100-8</pub-id><pub-id pub-id-type="pmid">30791958</pub-id></element-citation></ref><ref id="B164-cancers-11-01802"><label>164.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liang</surname><given-names>Y.</given-names></name><name><surname>Li</surname><given-names>Y.</given-names></name><name><surname>Song</surname><given-names>X.</given-names></name><name><surname>Zhang</surname><given-names>N.</given-names></name><name><surname>Sang</surname><given-names>Y.</given-names></name><name><surname>Zhang</surname><given-names>H.</given-names></name><name><surname>Liu</surname><given-names>Y.</given-names></name><name><surname>Chen</surname><given-names>B.</given-names></name><name><surname>Zhao</surname><given-names>W.</given-names></name><name><surname>Wang</surname><given-names>L.</given-names></name><etal></etal></person-group><article-title>Long noncoding RNA LINP1 acts as an oncogene and promotes chemoresistance in breast cancer</article-title><source>Cancer Biol. Ther.</source><year>2018</year><volume>19</volume><fpage>120</fpage><lpage>131</lpage><pub-id pub-id-type="doi">10.1080/15384047.2017.1394543</pub-id><pub-id pub-id-type="pmid">29293402</pub-id></element-citation></ref><ref id="B165-cancers-11-01802"><label>165.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Longley</surname><given-names>D.B.</given-names></name><name><surname>Harkin</surname><given-names>D.P.</given-names></name><name><surname>Johnston</surname><given-names>P.G.</given-names></name></person-group><article-title>5-fluorouracil: Mechanisms of action and clinical strategies</article-title><source>Nat. Rev. Cancer</source><year>2003</year><volume>3</volume><fpage>330</fpage><lpage>338</lpage><pub-id pub-id-type="doi">10.1038/nrc1074</pub-id><pub-id pub-id-type="pmid">12724731</pub-id></element-citation></ref><ref id="B166-cancers-11-01802"><label>166.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tacar</surname><given-names>O.</given-names></name><name><surname>Sriamornsak</surname><given-names>P.</given-names></name><name><surname>Dass</surname><given-names>C.R.</given-names></name></person-group><article-title>Doxorubicin: An update on anticancer molecular action, toxicity and novel drug delivery systems</article-title><source>J. Pharm. Pharmacol.</source><year>2013</year><volume>65</volume><fpage>157</fpage><lpage>170</lpage><pub-id pub-id-type="doi">10.1111/j.2042-7158.2012.01567.x</pub-id><pub-id pub-id-type="pmid">23278683</pub-id></element-citation></ref><ref id="B167-cancers-11-01802"><label>167.</label><element-citation publication-type="journal"><article-title>The Impact of lncRNA Dysregulation on Clinicopathology and Survival of Breast Cancer: A Systematic Review and Meta-analysis</article-title><source>Mol. Ther. Nucleic Acids</source><year>2018</year><volume>12</volume><fpage>359</fpage><lpage>369</lpage><pub-id pub-id-type="doi">10.1016/j.omtn.2018.05.018</pub-id><pub-id pub-id-type="pmid">30195774</pub-id></element-citation></ref><ref id="B168-cancers-11-01802"><label>168.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Sun</surname><given-names>M.</given-names></name><name><surname>Wu</surname><given-names>D.</given-names></name><name><surname>Zhou</surname><given-names>K.</given-names></name><name><surname>Li</surname><given-names>H.</given-names></name><name><surname>Gong</surname><given-names>X.</given-names></name><name><surname>Wei</surname><given-names>Q.</given-names></name><name><surname>Du</surname><given-names>M.</given-names></name><name><surname>Lei</surname><given-names>P.</given-names></name><name><surname>Zha</surname><given-names>J.</given-names></name><name><surname>Zhu</surname><given-names>H.</given-names></name></person-group><article-title>An eight-lncRNA signature predicts survival of breast cancer patients: A comprehensive study based on weighted gene co-expression network analysis and competing endogenous RNA network</article-title><source>Breast Cancer Res. Treat.</source><year>2019</year><volume>175</volume><fpage>59</fpage><lpage>75</lpage><pub-id pub-id-type="doi">10.1007/s10549-019-05147-6</pub-id><pub-id pub-id-type="pmid">30715658</pub-id></element-citation></ref><ref id="B169-cancers-11-01802"><label>169.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>K.</given-names></name><name><surname>Luo</surname><given-names>Z.</given-names></name><name><surname>Zhang</surname><given-names>Y.</given-names></name><name><surname>Zhang</surname><given-names>L.</given-names></name><name><surname>Wu</surname><given-names>L.</given-names></name><name><surname>Liu</surname><given-names>L.</given-names></name><name><surname>Yang</surname><given-names>J.</given-names></name><name><surname>Song</surname><given-names>X.</given-names></name><name><surname>Liu</surname><given-names>J.</given-names></name></person-group><article-title>Circulating lncRNA H19 in plasma as a novel biomarker for breast cancer</article-title><source>Cancer Biomark.</source><year>2016</year><volume>17</volume><fpage>187</fpage><lpage>194</lpage><pub-id pub-id-type="doi">10.3233/CBM-160630</pub-id><pub-id pub-id-type="pmid">27540977</pub-id></element-citation></ref><ref id="B170-cancers-11-01802"><label>170.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Han</surname><given-names>L.</given-names></name><name><surname>Ma</surname><given-names>P.</given-names></name><name><surname>Liu</surname><given-names>S.M.</given-names></name><name><surname>Zhou</surname><given-names>X.</given-names></name></person-group><article-title>Circulating long noncoding RNA GAS5 as a potential biomarker in breast cancer for assessing the surgical effects</article-title><source>Tumour Biol.</source><year>2016</year><volume>37</volume><fpage>6847</fpage><lpage>6854</lpage><pub-id pub-id-type="doi">10.1007/s13277-015-4568-7</pub-id><pub-id pub-id-type="pmid">26662314</pub-id></element-citation></ref><ref id="B171-cancers-11-01802"><label>171.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bai</surname><given-names>J.</given-names></name><name><surname>Zhao</surname><given-names>W.Y.</given-names></name><name><surname>Li</surname><given-names>W.J.</given-names></name><name><surname>Ying</surname><given-names>Z.W.</given-names></name><name><surname>Jiang</surname><given-names>D.Q.</given-names></name></person-group><article-title>Long noncoding RNA LINC00473 indicates a poor prognosis of breast cancer and accelerates tumor carcinogenesis by competing endogenous sponging miR-497</article-title><source>Eur. Rev. Med. Pharmacol. Sci.</source><year>2019</year><volume>23</volume><fpage>3410</fpage><lpage>3420</lpage><pub-id pub-id-type="pmid">31081095</pub-id></element-citation></ref><ref id="B172-cancers-11-01802"><label>172.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>X.M.</given-names></name><name><surname>Yang</surname><given-names>B.</given-names></name><name><surname>Han</surname><given-names>J.</given-names></name></person-group><article-title>Increased long noncoding RNA LINP1 expression and its prognostic significance in human breast cancer</article-title><source>Eur. Rev. Med. Pharmacol. Sci.</source><year>2018</year><volume>22</volume><fpage>8749</fpage><lpage>8754</lpage><pub-id pub-id-type="pmid">30575915</pub-id></element-citation></ref><ref id="B173-cancers-11-01802"><label>173.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Meng</surname><given-names>Y.</given-names></name><name><surname>Liu</surname><given-names>Y.L.</given-names></name><name><surname>Li</surname><given-names>K.</given-names></name><name><surname>Fu</surname><given-names>T.</given-names></name></person-group><article-title>Prognostic value of long non-coding RNA breast cancer anti-estrogen resistance 4 in human cancers: A meta-analysis</article-title><source>Medicine</source><year>2019</year><volume>98</volume><fpage>e15793</fpage><pub-id pub-id-type="doi">10.1097/MD.0000000000015793</pub-id><pub-id pub-id-type="pmid">31124974</pub-id></element-citation></ref><ref id="B174-cancers-11-01802"><label>174.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhao</surname><given-names>W.</given-names></name><name><surname>Wang</surname><given-names>Z.</given-names></name><name><surname>Fang</surname><given-names>X.</given-names></name><name><surname>Li</surname><given-names>N.</given-names></name><name><surname>Fang</surname><given-names>J.</given-names></name></person-group><article-title>Long noncoding RNA Breast cancer antiestrogen resistance 4 is associated with cancer progression and its significant prognostic value</article-title><source>J. Cell. Physiol.</source><year>2019</year><volume>234</volume><fpage>12956</fpage><lpage>12963</lpage><pub-id pub-id-type="doi">10.1002/jcp.27962</pub-id><pub-id pub-id-type="pmid">30537165</pub-id></element-citation></ref><ref id="B175-cancers-11-01802"><label>175.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lv</surname><given-names>M.</given-names></name><name><surname>Xu</surname><given-names>P.</given-names></name><name><surname>Wu</surname><given-names>Y.</given-names></name><name><surname>Huang</surname><given-names>L.</given-names></name><name><surname>Li</surname><given-names>W.</given-names></name><name><surname>Lv</surname><given-names>S.</given-names></name><name><surname>Wu</surname><given-names>X.</given-names></name><name><surname>Zeng</surname><given-names>X.</given-names></name><name><surname>Shen</surname><given-names>R.</given-names></name><name><surname>Jia</surname><given-names>X.</given-names></name><etal></etal></person-group><article-title>LncRNAs as new biomarkers to differentiate triple negative breast cancer from non-triple negative breast cancer</article-title><source>Oncotarget</source><year>2016</year><volume>7</volume><fpage>13047</fpage><lpage>13059</lpage><pub-id pub-id-type="doi">10.18632/oncotarget.7509</pub-id><pub-id pub-id-type="pmid">26910840</pub-id></element-citation></ref><ref id="B176-cancers-11-01802"><label>176.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>H.</given-names></name><name><surname>Zhang</surname><given-names>N.</given-names></name><name><surname>Liu</surname><given-names>Y.</given-names></name><name><surname>Su</surname><given-names>P.</given-names></name><name><surname>Liang</surname><given-names>Y.</given-names></name><name><surname>Li</surname><given-names>Y.</given-names></name><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Chen</surname><given-names>T.</given-names></name><name><surname>Song</surname><given-names>X.</given-names></name><name><surname>Sang</surname><given-names>Y.</given-names></name><etal></etal></person-group><article-title>Epigenetic Regulation of NAMPT by NAMPT-AS Drives Metastatic Progression in Triple-Negative Breast Cancer</article-title><source>Cancer Res.</source><year>2019</year><volume>79</volume><fpage>3347</fpage><lpage>3359</lpage><pub-id pub-id-type="doi">10.1158/0008-5472.CAN-18-3418</pub-id><pub-id pub-id-type="pmid">30940661</pub-id></element-citation></ref><ref id="B177-cancers-11-01802"><label>177.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>R.H.</given-names></name><name><surname>Chen</surname><given-names>M.</given-names></name><name><surname>Liu</surname><given-names>J.</given-names></name><name><surname>Shao</surname><given-names>C.C.</given-names></name><name><surname>Guo</surname><given-names>C.P.</given-names></name><name><surname>Wei</surname><given-names>X.L.</given-names></name><name><surname>Li</surname><given-names>Y.C.</given-names></name><name><surname>Huang</surname><given-names>W.H.</given-names></name><name><surname>Zhang</surname><given-names>G.J.</given-names></name></person-group><article-title>Long noncoding RNA ATB promotes the epithelial-mesenchymal transition by upregulating the miR-200c/Twist1 axe and predicts poor prognosis in breast cancer</article-title><source>Cell Death Dis.</source><year>2018</year><volume>9</volume><fpage>1171</fpage><pub-id pub-id-type="doi">10.1038/s41419-018-1210-9</pub-id><pub-id pub-id-type="pmid">30518916</pub-id></element-citation></ref><ref id="B178-cancers-11-01802"><label>178.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Fu</surname><given-names>J.</given-names></name><name><surname>Dong</surname><given-names>G.</given-names></name><name><surname>Shi</surname><given-names>H.</given-names></name><name><surname>Zhang</surname><given-names>J.</given-names></name><name><surname>Ning</surname><given-names>Z.</given-names></name><name><surname>Bao</surname><given-names>X.</given-names></name><name><surname>Liu</surname><given-names>C.</given-names></name><name><surname>Hu</surname><given-names>J.</given-names></name><name><surname>Liu</surname><given-names>M.</given-names></name><name><surname>Xiong</surname><given-names>B.</given-names></name></person-group><article-title>LncRNA MIR503HG inhibits cell migration and invasion via miR-103/OLFM4 axis in triple negative breast cancer</article-title><source>J. Cell. Mol. Med.</source><year>2019</year><volume>23</volume><fpage>4738</fpage><lpage>4745</lpage><pub-id pub-id-type="doi">10.1111/jcmm.14344</pub-id><pub-id pub-id-type="pmid">31062436</pub-id></element-citation></ref><ref id="B179-cancers-11-01802"><label>179.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shore</surname><given-names>A.N.</given-names></name><name><surname>Rosen</surname><given-names>J.M.</given-names></name></person-group><article-title>Regulation of mammary epithelial cell homeostasis by lncRNAs</article-title><source>Int. J. Biochem. Cell Biol.</source><year>2014</year><volume>54</volume><fpage>318</fpage><lpage>330</lpage><pub-id pub-id-type="doi">10.1016/j.biocel.2014.03.012</pub-id><pub-id pub-id-type="pmid">24680897</pub-id></element-citation></ref><ref id="B180-cancers-11-01802"><label>180.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chen</surname><given-names>M.</given-names></name><name><surname>Zhuang</surname><given-names>C.</given-names></name><name><surname>Liu</surname><given-names>Y.</given-names></name><name><surname>Li</surname><given-names>J.</given-names></name><name><surname>Dai</surname><given-names>F.</given-names></name><name><surname>Xia</surname><given-names>M.</given-names></name><name><surname>Zhan</surname><given-names>Y.</given-names></name><name><surname>Lin</surname><given-names>J.</given-names></name><name><surname>Chen</surname><given-names>Z.</given-names></name><name><surname>He</surname><given-names>A.</given-names></name><etal></etal></person-group><article-title>Tetracycline-inducible shRNA targeting antisense long non-coding RNA HIF1A-AS2 represses the malignant phenotypes of bladder cancer</article-title><source>Cancer Lett.</source><year>2016</year><volume>376</volume><fpage>155</fpage><lpage>164</lpage><pub-id pub-id-type="doi">10.1016/j.canlet.2016.03.037</pub-id><pub-id pub-id-type="pmid">27018306</pub-id></element-citation></ref><ref id="B181-cancers-11-01802"><label>181.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Campbell</surname><given-names>P.</given-names></name><name><surname>Yachida</surname><given-names>S.</given-names></name><name><surname>Mudie</surname><given-names>L.</given-names></name><name><surname>Stephens</surname><given-names>P.</given-names></name><name><surname>Pleasance</surname><given-names>E.</given-names></name><name><surname>Stebbings</surname><given-names>L.</given-names></name><name><surname>Morsberger</surname><given-names>L.</given-names></name><name><surname>Latimer</surname><given-names>C.</given-names></name><name><surname>McLaren</surname><given-names>S.</given-names></name><name><surname>Lin</surname><given-names>M.</given-names></name><etal></etal></person-group><article-title>The patterns and dynamics of genomic instability in metastatic pancreatic cancer</article-title><source>Nature</source><year>2010</year><volume>467</volume><fpage>1109</fpage><lpage>1113</lpage><pub-id pub-id-type="doi">10.1038/nature09460</pub-id><pub-id pub-id-type="pmid">20981101</pub-id></element-citation></ref><ref id="B182-cancers-11-01802"><label>182.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wu</surname><given-names>X.</given-names></name><name><surname>Northcott</surname><given-names>P.</given-names></name><name><surname>Dubuc</surname><given-names>A.</given-names></name><name><surname>Dupuy</surname><given-names>A.</given-names></name><name><surname>Shih</surname><given-names>D.</given-names></name><name><surname>Witt</surname><given-names>H.</given-names></name><name><surname>Croul</surname><given-names>S.</given-names></name><name><surname>Bouffet</surname><given-names>E.</given-names></name><name><surname>Fults</surname><given-names>D.</given-names></name><name><surname>Eberhart</surname><given-names>C.</given-names></name><etal></etal></person-group><article-title>Clonal selection drives genetic divergence of metastatic medulloblastoma</article-title><source>Nature</source><year>2012</year><volume>482</volume><fpage>529</fpage><lpage>533</lpage><pub-id pub-id-type="doi">10.1038/nature10825</pub-id><pub-id pub-id-type="pmid">22343890</pub-id></element-citation></ref><ref id="B183-cancers-11-01802"><label>183.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mizushima</surname><given-names>N.</given-names></name><name><surname>Yoshimori</surname><given-names>T.</given-names></name><name><surname>Ohsumi</surname><given-names>Y.</given-names></name></person-group><article-title>The role of Atg proteins in autophagosome formation</article-title><source>Annu. Rev. Cell. Dev. Biol.</source><year>2011</year><volume>27</volume><fpage>107</fpage><lpage>132</lpage><pub-id pub-id-type="doi">10.1146/annurev-cellbio-092910-154005</pub-id><pub-id pub-id-type="pmid">21801009</pub-id></element-citation></ref><ref id="B184-cancers-11-01802"><label>184.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kenific</surname><given-names>C.M.</given-names></name><name><surname>Thorburn</surname><given-names>A.</given-names></name><name><surname>Debnath</surname><given-names>J.</given-names></name></person-group><article-title>Autophagy and metastasis: Another double-edged sword</article-title><source>Curr. Opin. Cell Biol.</source><year>2010</year><volume>22</volume><fpage>241</fpage><lpage>245</lpage><pub-id pub-id-type="doi">10.1016/j.ceb.2009.10.008</pub-id><pub-id pub-id-type="pmid">19945838</pub-id></element-citation></ref><ref id="B185-cancers-11-01802"><label>185.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Moraes</surname><given-names>L.A.</given-names></name><name><surname>Kar</surname><given-names>S.</given-names></name><name><surname>Foo</surname><given-names>S.L.</given-names></name><name><surname>Gu</surname><given-names>T.</given-names></name><name><surname>Toh</surname><given-names>Y.Q.</given-names></name><name><surname>Ampomah</surname><given-names>P.B.</given-names></name><name><surname>Sachaphibulkij</surname><given-names>K.</given-names></name><name><surname>Yap</surname><given-names>G.</given-names></name><name><surname>Zharkova</surname><given-names>O.</given-names></name><name><surname>Lukman</surname><given-names>H.M.</given-names></name><etal></etal></person-group><article-title>Annexin-A1 enhances breast cancer growth and migration by promoting alternative macrophage polarization in the tumour microenvironment</article-title><source>Sci. Rep.</source><year>2017</year><volume>7</volume><fpage>17925</fpage><pub-id pub-id-type="doi">10.1038/s41598-017-17622-5</pub-id><pub-id pub-id-type="pmid">29263330</pub-id></element-citation></ref><ref id="B186-cancers-11-01802"><label>186.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gu</surname><given-names>J.</given-names></name><name><surname>Wang</surname><given-names>Y.</given-names></name><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Zhou</surname><given-names>D.</given-names></name><name><surname>Wang</surname><given-names>X.</given-names></name><name><surname>Zhou</surname><given-names>M.</given-names></name><name><surname>He</surname><given-names>Z.</given-names></name></person-group><article-title>Effect of the LncRNA GAS5-MiR-23a-ATG3 Axis in Regulating Autophagy in Patients with Breast Cancer</article-title><source>Cell. Physiol. Biochem.</source><year>2018</year><volume>48</volume><fpage>194</fpage><lpage>207</lpage><pub-id pub-id-type="doi">10.1159/000491718</pub-id><pub-id pub-id-type="pmid">30007957</pub-id></element-citation></ref><ref id="B187-cancers-11-01802"><label>187.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ruiz</surname><given-names>A.</given-names></name><name><surname>Rockfield</surname><given-names>S.</given-names></name><name><surname>Taran</surname><given-names>N.</given-names></name><name><surname>Haller</surname><given-names>E.</given-names></name><name><surname>Engelman</surname><given-names>R.</given-names></name><name><surname>Flores</surname><given-names>I.</given-names></name><name><surname>Panina-Bordignon</surname><given-names>P.</given-names></name><name><surname>Nanjundan</surname><given-names>M.</given-names></name></person-group><article-title>Effect of hydroxychloroquine and characterization of autophagy in a mouse model of endometriosis</article-title><source>Cell Death Dis.</source><year>2016</year><volume>7</volume><fpage>e2059</fpage><pub-id pub-id-type="doi">10.1038/cddis.2015.361</pub-id><pub-id pub-id-type="pmid">26775710</pub-id></element-citation></ref><ref id="B188-cancers-11-01802"><label>188.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cao</surname><given-names>Z.</given-names></name><name><surname>Livas</surname><given-names>T.</given-names></name><name><surname>Kyprianou</surname><given-names>N.</given-names></name></person-group><article-title>Anoikis and EMT: Lethal “Liaisons” during Cancer Progression</article-title><source>Crit. Rev. Oncog.</source><year>2016</year><volume>21</volume><fpage>155</fpage><lpage>168</lpage><pub-id pub-id-type="doi">10.1615/CritRevOncog.2016016955</pub-id><pub-id pub-id-type="pmid">27915969</pub-id></element-citation></ref><ref id="B189-cancers-11-01802"><label>189.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lu</surname><given-names>J.</given-names></name><name><surname>Tan</surname><given-names>M.</given-names></name><name><surname>Cai</surname><given-names>Q.</given-names></name></person-group><article-title>The Warburg effect in tumor progression: Mitochondrial oxidative metabolism as an anti-metastasis mechanism</article-title><source>Cancer Lett.</source><year>2015</year><volume>356</volume><fpage>156</fpage><lpage>164</lpage><pub-id pub-id-type="doi">10.1016/j.canlet.2014.04.001</pub-id><pub-id pub-id-type="pmid">24732809</pub-id></element-citation></ref><ref id="B190-cancers-11-01802"><label>190.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>X.</given-names></name><name><surname>Fu</surname><given-names>Q.</given-names></name><name><surname>Li</surname><given-names>S.</given-names></name><name><surname>Liang</surname><given-names>N.</given-names></name><name><surname>Li</surname><given-names>F.</given-names></name><name><surname>Li</surname><given-names>C.</given-names></name><name><surname>Sui</surname><given-names>C.</given-names></name><name><surname>Dionigi</surname><given-names>G.</given-names></name><name><surname>Sun</surname><given-names>H.</given-names></name></person-group><article-title>LncRNA FOXD2-AS1 Functions as a Competing Endogenous RNA to Regulate TERT Expression by Sponging miR-7-5p in Thyroid Cancer</article-title><source>Front. Endocrinol.</source><year>2019</year><volume>10</volume><fpage>207</fpage><pub-id pub-id-type="doi">10.3389/fendo.2019.00207</pub-id></element-citation></ref><ref id="B191-cancers-11-01802"><label>191.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gordon</surname><given-names>M.</given-names></name><name><surname>Babbs</surname><given-names>B.</given-names></name><name><surname>Cochrane</surname><given-names>D.</given-names></name><name><surname>Bitler</surname><given-names>B.</given-names></name><name><surname>Richer</surname><given-names>J.</given-names></name></person-group><article-title>The long non-coding RNA MALAT1 promotes ovarian cancer progression by regulating RBFOX2-mediated alternative splicing</article-title><source>Mol. Carcinog.</source><year>2019</year><volume>58</volume><fpage>196</fpage><lpage>205</lpage><pub-id pub-id-type="doi">10.1002/mc.22919</pub-id><pub-id pub-id-type="pmid">30294913</pub-id></element-citation></ref><ref id="B192-cancers-11-01802"><label>192.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Seitz</surname><given-names>A.</given-names></name><name><surname>Christensen</surname><given-names>L.</given-names></name><name><surname>Christensen</surname><given-names>E.</given-names></name><name><surname>Faarkrog</surname><given-names>K.</given-names></name><name><surname>Ostenfeld</surname><given-names>M.</given-names></name><name><surname>Hedegaard</surname><given-names>J.</given-names></name><name><surname>Nordentoft</surname><given-names>I.</given-names></name><name><surname>Nielsen</surname><given-names>M.</given-names></name><name><surname>Palmfeldt</surname><given-names>J.</given-names></name><name><surname>Thomson</surname><given-names>M.</given-names></name><etal></etal></person-group><article-title>Profiling of long non-coding RNAs identifies LINC00958 and LINC01296 as candidate oncogenes in bladder cancer</article-title><source>Sci. Rep.</source><year>2017</year><volume>7</volume><fpage>395</fpage><pub-id pub-id-type="doi">10.1038/s41598-017-00327-0</pub-id><pub-id pub-id-type="pmid">28341852</pub-id></element-citation></ref><ref id="B193-cancers-11-01802"><label>193.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dai</surname><given-names>X.</given-names></name><name><surname>Li</surname><given-names>T.</given-names></name><name><surname>Bai</surname><given-names>Z.</given-names></name><name><surname>Yang</surname><given-names>Y.</given-names></name><name><surname>Liu</surname><given-names>X.</given-names></name><name><surname>Zhan</surname><given-names>J.</given-names></name><name><surname>Shi</surname><given-names>B.</given-names></name></person-group><article-title>Breast cancer intrinsic subtype classification, clinical use and future trends</article-title><source>Am. J. Cancer Res.</source><year>2015</year><volume>5</volume><fpage>2929</fpage><lpage>2943</lpage><pub-id pub-id-type="pmid">26693050</pub-id></element-citation></ref><ref id="B194-cancers-11-01802"><label>194.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Heimes</surname><given-names>A.S.</given-names></name><name><surname>Madjar</surname><given-names>K.</given-names></name><name><surname>Edlund</surname><given-names>K.</given-names></name><name><surname>Battista</surname><given-names>M.J.</given-names></name><name><surname>Almstedt</surname><given-names>K.</given-names></name><name><surname>Elger</surname><given-names>T.</given-names></name><name><surname>Krajnak</surname><given-names>S.</given-names></name><name><surname>Rahnenführer</surname><given-names>J.</given-names></name><name><surname>Brenner</surname><given-names>W.</given-names></name><name><surname>Hasenburg</surname><given-names>A.</given-names></name></person-group><article-title>Subtype-specific prognostic impact of different immune signatures in node-negative breast cancer</article-title><source>Breast Cancer Res. Treat.</source><year>2017</year><volume>14</volume><fpage>1</fpage><lpage>8</lpage><pub-id pub-id-type="doi">10.1007/s10549-017-4327-0</pub-id><pub-id pub-id-type="pmid">28585074</pub-id></element-citation></ref><ref id="B195-cancers-11-01802"><label>195.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mathias</surname><given-names>C.</given-names></name><name><surname>Zambalde</surname><given-names>E.</given-names></name><name><surname>Rask</surname><given-names>P.</given-names></name><name><surname>Gradia</surname><given-names>D.</given-names></name><name><surname>de Oliveira</surname><given-names>J.</given-names></name></person-group><article-title>Long non-coding RNAs differential expression in breast cancer subtypes: What do we know?</article-title><source>Clin. Genet.</source><year>2019</year><volume>95</volume><fpage>558</fpage><lpage>568</lpage><pub-id pub-id-type="doi">10.1111/cge.13502</pub-id><pub-id pub-id-type="pmid">30614523</pub-id></element-citation></ref><ref id="B196-cancers-11-01802"><label>196.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Bhan</surname><given-names>A.</given-names></name><name><surname>Hussain</surname><given-names>I.</given-names></name><name><surname>Ansari</surname><given-names>K.I.</given-names></name><name><surname>Kasiri</surname><given-names>S.</given-names></name><name><surname>Bashyal</surname><given-names>A.</given-names></name><name><surname>Mandal</surname><given-names>S.S.</given-names></name></person-group><article-title>Antisense Transcript Long Noncoding RNA (lncRNA) HOTAIR is Transcriptionally Induced by Estradiol</article-title><source>J. Mol. Biol.</source><year>2013</year><volume>425</volume><fpage>3707</fpage><lpage>3722</lpage><pub-id pub-id-type="doi">10.1016/j.jmb.2013.01.022</pub-id><pub-id pub-id-type="pmid">23375982</pub-id></element-citation></ref><ref id="B197-cancers-11-01802"><label>197.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>F.</given-names></name><name><surname>Lyu</surname><given-names>S.</given-names></name><name><surname>Dong</surname><given-names>S.</given-names></name><name><surname>Liu</surname><given-names>Y.</given-names></name><name><surname>Zhang</surname><given-names>X.</given-names></name><name><surname>Wang</surname><given-names>O.</given-names></name></person-group><article-title>Expression profile analysis of long noncoding RNA in HER-2-enriched subtype breast cancer by next-generation sequencing and bioinformatics</article-title><source>Onco Targets Ther.</source><year>2016</year><volume>9</volume><fpage>761</fpage><lpage>772</lpage><pub-id pub-id-type="doi">10.2147/OTT.S97664</pub-id><pub-id pub-id-type="pmid">26929647</pub-id></element-citation></ref><ref id="B198-cancers-11-01802"><label>198.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lehmann</surname><given-names>B.</given-names></name><name><surname>Bauer</surname><given-names>J.</given-names></name><name><surname>Chen</surname><given-names>X.</given-names></name><name><surname>Sanders</surname><given-names>M.</given-names></name><name><surname>Chakravarthy</surname><given-names>A.</given-names></name><name><surname>Shyr</surname><given-names>Y.</given-names></name><name><surname>Pietenpol</surname><given-names>J.</given-names></name></person-group><article-title>Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies</article-title><source>J. Clin. Investig.</source><year>2011</year><volume>121</volume><fpage>2750</fpage><lpage>2767</lpage><pub-id pub-id-type="doi">10.1172/JCI45014</pub-id><pub-id pub-id-type="pmid">21633166</pub-id></element-citation></ref><ref id="B199-cancers-11-01802"><label>199.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>E.</given-names></name><name><surname>Liu</surname><given-names>Z.</given-names></name><name><surname>Zhou</surname><given-names>Y.</given-names></name></person-group><article-title>Carboplatin-docetaxel-induced activity against ovarian cancer is dependent on up-regulated lncRNA PVT1</article-title><source>Int. J. Clin. Exp. Pathol.</source><year>2014</year><volume>8</volume><fpage>3803</fpage></element-citation></ref><ref id="B200-cancers-11-01802"><label>200.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Martin</surname><given-names>D.</given-names></name><name><surname>Smith</surname><given-names>C.L.</given-names></name></person-group><article-title>Ligand-independent interactions of p160/steroid receptor coactivators and CREB-binding protein (CBP) with estrogen receptor-alpha: Regulation by phosphorylation sites in the A/B region depends on other receptor domains</article-title><source>Mol. Endocrinol.</source><year>2003</year><volume>17</volume><fpage>1296</fpage><lpage>1314</lpage><pub-id pub-id-type="pmid">12714702</pub-id></element-citation></ref><ref id="B201-cancers-11-01802"><label>201.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhao</surname><given-names>Z.</given-names></name><name><surname>Chen</surname><given-names>C.</given-names></name><name><surname>Liu</surname><given-names>Y.</given-names></name><name><surname>Wu</surname><given-names>C.</given-names></name></person-group><article-title>17β-Estradiol treatment inhibits breast cell proliferation, migration and invasion by decreasing MALAT-1 RNA level</article-title><source>Biochem. Biophys. Res. Commun.</source><year>2014</year><volume>445</volume><fpage>388</fpage><lpage>393</lpage><pub-id pub-id-type="doi">10.1016/j.bbrc.2014.02.006</pub-id><pub-id pub-id-type="pmid">24525122</pub-id></element-citation></ref><ref id="B202-cancers-11-01802"><label>202.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Gupta</surname><given-names>P.B.</given-names></name><name><surname>Pastushenko</surname><given-names>I.</given-names></name><name><surname>Skibinski</surname><given-names>A.</given-names></name><name><surname>Blanpain</surname><given-names>C.</given-names></name><name><surname>Kuperwasser</surname><given-names>C.</given-names></name></person-group><article-title>Phenotypic Plasticity: Driver of Cancer Initiation, Progression, and Therapy Resistance</article-title><source>Cell Stem Cell</source><year>2019</year><volume>24</volume><fpage>65</fpage><lpage>78</lpage><pub-id pub-id-type="doi">10.1016/j.stem.2018.11.011</pub-id><pub-id pub-id-type="pmid">30554963</pub-id></element-citation></ref><ref id="B203-cancers-11-01802"><label>203.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pastushenko</surname><given-names>I.</given-names></name><name><surname>Blanpain</surname><given-names>C.</given-names></name></person-group><article-title>EMT Transition States during Tumor Progression and Metastasis</article-title><source>Trends Cell Biol.</source><year>2019</year><volume>29</volume><fpage>212</fpage><lpage>226</lpage><pub-id pub-id-type="doi">10.1016/j.tcb.2018.12.001</pub-id><pub-id pub-id-type="pmid">30594349</pub-id></element-citation></ref><ref id="B204-cancers-11-01802"><label>204.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Norouzi</surname><given-names>S.</given-names></name><name><surname>Gorgi Valokala</surname><given-names>M.</given-names></name><name><surname>Mosaffa</surname><given-names>F.</given-names></name><name><surname>Zirak</surname><given-names>M.</given-names></name><name><surname>Zamani</surname><given-names>P.</given-names></name><name><surname>Behravan</surname><given-names>J.</given-names></name></person-group><article-title>Crosstalk in cancer resistance and metastasis</article-title><source>Crit. Rev. Oncol. Hematol.</source><year>2018</year><volume>132</volume><fpage>145</fpage><lpage>153</lpage><pub-id pub-id-type="doi">10.1016/j.critrevonc.2018.09.017</pub-id><pub-id pub-id-type="pmid">30447920</pub-id></element-citation></ref><ref id="B205-cancers-11-01802"><label>205.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lawson</surname><given-names>D.</given-names></name><name><surname>Kessenbrock</surname><given-names>K.</given-names></name><name><surname>Davis</surname><given-names>R.</given-names></name><name><surname>Pervolarakis</surname><given-names>N.</given-names></name><name><surname>Werb</surname><given-names>Z.</given-names></name></person-group><article-title>Tumour heterogeneity and metastasis at single-cell resolution</article-title><source>Nat. Cell Biol.</source><year>2018</year><volume>20</volume><fpage>1349</fpage><lpage>1360</lpage><pub-id pub-id-type="doi">10.1038/s41556-018-0236-7</pub-id><pub-id pub-id-type="pmid">30482943</pub-id></element-citation></ref><ref id="B206-cancers-11-01802"><label>206.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wang</surname><given-names>Q.</given-names></name><name><surname>Fan</surname><given-names>H.</given-names></name><name><surname>Liu</surname><given-names>Y.</given-names></name><name><surname>Yin</surname><given-names>Z.</given-names></name><name><surname>Cai</surname><given-names>H.</given-names></name><name><surname>Liu</surname><given-names>J.</given-names></name><name><surname>Wang</surname><given-names>Z.</given-names></name><name><surname>Shao</surname><given-names>M.</given-names></name><name><surname>Sun</surname><given-names>X.</given-names></name><name><surname>Diao</surname><given-names>J.</given-names></name><etal></etal></person-group><article-title>Curcumin enhances the radiosensitivity in nasopharyngeal carcinoma cells involving the reversal of differentially expressed long non-coding RNAs</article-title><source>Int. J. Oncol.</source><year>2014</year><volume>44</volume><fpage>858</fpage><lpage>864</lpage><pub-id pub-id-type="doi">10.3892/ijo.2013.2237</pub-id><pub-id pub-id-type="pmid">24379026</pub-id></element-citation></ref><ref id="B207-cancers-11-01802"><label>207.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hu</surname><given-names>X.</given-names></name><name><surname>Ding</surname><given-names>D.</given-names></name><name><surname>Zhang</surname><given-names>J.</given-names></name><name><surname>Cui</surname><given-names>J.</given-names></name></person-group><article-title>Knockdown of lncRNA HOTAIR sensitizes breast cancer cells to ionizing radiation through activating miR-218</article-title><source>Biosci. Rep.</source><year>2019</year><volume>39</volume><pub-id pub-id-type="doi">10.1042/BSR20181038</pub-id></element-citation></ref><ref id="B208-cancers-11-01802"><label>208.</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>Y.</given-names></name><name><surname>He</surname><given-names>Q.</given-names></name><name><surname>Hu</surname><given-names>Z.</given-names></name><name><surname>Feng</surname><given-names>Y.</given-names></name><name><surname>Fan</surname><given-names>L.</given-names></name><name><surname>Tang</surname><given-names>Z.</given-names></name><name><surname>Yuan</surname><given-names>J.</given-names></name><name><surname>Shan</surname><given-names>W.</given-names></name><name><surname>Li</surname><given-names>C.</given-names></name><name><surname>Hu</surname><given-names>X.</given-names></name><etal></etal></person-group><article-title>Long noncoding RNA LINP1 regulates repair of DNA double-strand breaks in triple-negative breast cancer</article-title><source>Nat. Struct. Mol. Biol.</source><year>2016</year><volume>23</volume><fpage>522</fpage><lpage>530</lpage><pub-id pub-id-type="doi">10.1038/nsmb.3211</pub-id><pub-id pub-id-type="pmid">27111890</pub-id></element-citation></ref></ref-list></back><floats-group><fig id="cancers-11-01802-f001" orientation="portrait" position="float"><label>Figure 1</label><caption><p>LncRNAs and prognosis of BC patients. Here both up-regulated lncRNA in BC tissue (HOTAIR, TINCR, LIP1, MALAT1, and LINC000473) and circulating lncRNA in plasma (HOTAIR, H19, and GAS5) predict poor prognosis of BC patients. The red or white up arrows respectively refer to up-regulation of the relevant lncRNA in BC patients’ tissue or plasma.</p></caption><graphic xlink:href="cancers-11-01802-g001"></graphic></fig><fig id="cancers-11-01802-f002" orientation="portrait" position="float"><label>Figure 2</label><caption><p>LncRNAs as biomarkers for diagnosis and prognosis of TNBC patients. Up-regulated expression of DANCR, NAMPT-AS, ATB, and HIF1A-AS2 predict poor prognosis of TNBC patients. Down-regulated expression of MIR503HG predicts poor prognosis of TNBC patients. Red up arrows refer to up-regulation of the relevant lncRNA. Blue down arrows refer to down-regulation of the relevant lncRNA.</p></caption><graphic xlink:href="cancers-11-01802-g002"></graphic></fig><table-wrap id="cancers-11-01802-t001" orientation="portrait" position="float"><object-id pub-id-type="pii">cancers-11-01802-t001_Table 1</object-id><label>Table 1</label><caption><p>Dual effects of lncRNAs in various stage of BC progression.</p></caption><table frame="hsides" rules="groups"><thead><tr><th colspan="2" align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1">Function</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">LncRNA</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Ensembl ID</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Subcellular Localization</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Signaling Axis and Pathway</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">References</th></tr></thead><tbody><tr><td rowspan="26" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">Promote</td><td rowspan="10" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">invasion and migration of BC cells</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">DANCR</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">ENSG00000226950</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">DANCR/EZH2/ABCG2</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B27-cancers-11-01802" ref-type="bibr">27</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">DANCR/miRNA-216a-5p</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B30-cancers-11-01802" ref-type="bibr">30</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">H19</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000130600</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">H19/miR-152/DNMT</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B36-cancers-11-01802" ref-type="bibr">36</xref>]</td></tr><tr><td rowspan="3" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">HOTAIR</td><td rowspan="3" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">ENSG00000228630</td><td rowspan="3" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">Cytoplasm and nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HOTAIR/P53/AKT/JNK/MMPs</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B44-cancers-11-01802" ref-type="bibr">44</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HOTAIR/AKT/mTOR</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B45-cancers-11-01802" ref-type="bibr">45</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HOTAIR/miR-20a-5p/HMGA2</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B46-cancers-11-01802" ref-type="bibr">46</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LINC00152</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000222041</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LINC00152/BRCA1/PTEN</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B48-cancers-11-01802" ref-type="bibr">48</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LINC00461</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000245526</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LINC00461/miR-30a-5p/integrin β3</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B53-cancers-11-01802" ref-type="bibr">53</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">NEAT1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000245532</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">NEAT1/miR-448/ZEB1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B58-cancers-11-01802" ref-type="bibr">58</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LINC01857</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000224137</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LINC01857/CREBBP/H3K27Ac and CREB1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B60-cancers-11-01802" ref-type="bibr">60</xref>]</td></tr><tr><td rowspan="6" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">distant metastasis of BC cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">H19</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000130600</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">H19/let-7b/CYTH3/ARF</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B63-cancers-11-01802" ref-type="bibr">63</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HOTAIR</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000228630</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm and nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">TGF-β1/CDK5/HOTAIR/H3K27</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B69-cancers-11-01802" ref-type="bibr">69</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HIF1A-AS2</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000258667</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">unclear</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B180-cancers-11-01802" ref-type="bibr">180</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">RP1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENST00000420172</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">KLF5/RP1/p27kip1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B76-cancers-11-01802" ref-type="bibr">76</xref>]</td></tr><tr><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">MALAT1</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">ENSG00000251562</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MALAT1/miR-1/slug</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B80-cancers-11-01802" ref-type="bibr">80</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MALAT1/miR-129-5p</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B85-cancers-11-01802" ref-type="bibr">85</xref>]</td></tr><tr><td rowspan="9" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">stemness of BC cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">TUNAR</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000250366</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">TUNAR/SOX2</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B134-cancers-11-01802" ref-type="bibr">134</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LINC00511</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000227036</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LINC00511/miR-185-3p/E2F1/Nanog</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B139-cancers-11-01802" ref-type="bibr">139</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">lncRNA-Hh</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">lncRNA-Hh/GAS1/SOX2/OCT4</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B136-cancers-11-01802" ref-type="bibr">136</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">FEZF1-AS1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000230316</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">FEZF1-AS1/miR-30a/Nanog</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B138-cancers-11-01802" ref-type="bibr">138</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">FGF13-AS1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000226031</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">FGF13-AS1/IGF2BPs/Myc</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B140-cancers-11-01802" ref-type="bibr">140</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ES1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000226673</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ES1/Oct4/Sox2/miR-302</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B135-cancers-11-01802" ref-type="bibr">135</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">RP1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENST00000420172</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">RP1/p-4E-BP1/eIF4E/p27kip1/Snail1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B76-cancers-11-01802" ref-type="bibr">76</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">H19</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000130600</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">H19/let-7/HIF-1/PDK1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B143-cancers-11-01802" ref-type="bibr">143</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HOTAIR</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000228630</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm and nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">HOTAIR/miR-34a/SOX2</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B137-cancers-11-01802" ref-type="bibr">137</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">BC angiogenesis</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MALAT1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000251562</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MALAT1/miR-145/VEGF</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B148-cancers-11-01802" ref-type="bibr">148</xref>]</td></tr><tr><td rowspan="16" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">Inhibit</td><td rowspan="8" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">invasion and migration of BC cells</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">GAS5</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">ENSG00000234741</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">Cytoplasm and nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">GAS5/miR-21/RISC</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B88-cancers-11-01802" ref-type="bibr">88</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">GAS5/miR-196a-5p/FOXO1/PI3K/AKT</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B89-cancers-11-01802" ref-type="bibr">89</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MT1JP</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000255986</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MT1JP/miR-24-3p/Wnt/β-catenin</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B161-cancers-11-01802" ref-type="bibr">161</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">NKILA</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000278709</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">NKILA/NF-ĸB/MMPs</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B100-cancers-11-01802" ref-type="bibr">100</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">NEF</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">NEF/miRNA-155</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B97-cancers-11-01802" ref-type="bibr">97</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LET</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">unclear</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B101-cancers-11-01802" ref-type="bibr">101</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">TFAP2A-AS1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">TFAP2A-AS1/miR-933/SMAD2</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B102-cancers-11-01802" ref-type="bibr">102</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">LncKLHDC7B</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">unclear</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B103-cancers-11-01802" ref-type="bibr">103</xref>]</td></tr><tr><td rowspan="6" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">distant metastasis of BC cells</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">MALAT1</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">ENSG00000251562</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">PTEN/microRNA/MALAT1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B109-cancers-11-01802" ref-type="bibr">109</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MALAT1/YAP-TEAD</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B107-cancers-11-01802" ref-type="bibr">107</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MEG3</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000214548</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">miR-506/SP3/SP1/DNMT1/MEG3</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B111-cancers-11-01802" ref-type="bibr">111</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">NLIPMT</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Cytoplasm</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">NLIPMT/GSK3β and EMT proteins</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B115-cancers-11-01802" ref-type="bibr">115</xref>]</td></tr><tr><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">XIST</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">ENSG00000229807</td><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">XIST/MSN/c-Met</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B125-cancers-11-01802" ref-type="bibr">125</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">XIST/miR-155/CDX1</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B123-cancers-11-01802" ref-type="bibr">123</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">stemness of BC cells</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">XIST</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000229807</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">XIST/MSN/EMT proteins</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B125-cancers-11-01802" ref-type="bibr">125</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">BC angiogenesis</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MEG3</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">ENSG00000214548</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Nucleus</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">MEG3/AKT signaling</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B150-cancers-11-01802" ref-type="bibr">150</xref>]</td></tr></tbody></table></table-wrap></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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