Knockdown of TRIM65 inhibits autophagy and cisplatin resistance in A549/DDP cells by regulating miR-138-5p/ATG7
Identifieur interne : 000649 ( Pmc/Checkpoint ); précédent : 000648; suivant : 000650Knockdown of TRIM65 inhibits autophagy and cisplatin resistance in A549/DDP cells by regulating miR-138-5p/ATG7
Auteurs : Xufeng Pan ; Yong Chen ; Yuzhou Shen ; Jicheng TantaiSource :
- Cell Death & Disease [ 2041-4889 ] ; 2019.
Abstract
Cisplatin resistance is the main cause of treatment failure in patients with non-small-cell lung cancer (NSCLC). Autophagy is a key mechanism of resistance to chemotherapy. Given that tripartite motif (TRIM)-containing proteins are involved in the regulation of autophagy and chemoresistance, we aimed to study the functions of TRIM protein members in autophagy-mediated chemoresistance of NSCLC. We found that TRIM65 was significantly increased in cisplatin-resistant NSCLC cell line (A549/DDP) as compared to the parental cell line (A549). Knockdown of TRIM65 can enhance cisplatin-induced apoptosis and inhibit autophagy in A549/DDP cells, as indicated by Annexin V/PI staining, caspase3 activity test, and LC3-II immunofluorescence staining. Additionally, knockdown of TRIM65 significantly decreased the expression of an important autophagy mediator, ATG7, which was a potential target of miR-138-5p. miR-138-5p inhibitor significantly abolished the effects of TRIM65 knockdown on autophagy and cisplatin-induced apoptosis. Moreover, TRIM65 induced the ubiquitination and degradation of TNRC6A, resulting in the suppressed expression of miR-138-5p. TRIM65 knockdown inhibited the growth of tumors derived from A549/DDP cells. Furthermore, cisplatin-resistant NSCLC tissues displayed higher expression of TRIM65 mRNA and lower expression of miR-138-5p as compared to cisplatin non-resistant ones. miR-138-5p expression was negatively correlated with TRIM65 mRNA in NSCLC tissues. Collectively, the present study indicates that TRIM65 knockdown attenuates autophagy and cisplatin resistance in A549/DDP cells via regulating miR-138-5p.
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DOI: 10.1038/s41419-019-1660-8
PubMed: 31160576
PubMed Central: 6546683
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Knockdown of TRIM65 inhibits autophagy and cisplatin resistance in A549/DDP cells by regulating miR-138-5p/ATG7</title><author><name sortKey="Pan, Xufeng" sort="Pan, Xufeng" uniqKey="Pan X" first="Xufeng" last="Pan">Xufeng Pan</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Chen, Yong" sort="Chen, Yong" uniqKey="Chen Y" first="Yong" last="Chen">Yong Chen</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Shen, Yuzhou" sort="Shen, Yuzhou" uniqKey="Shen Y" first="Yuzhou" last="Shen">Yuzhou Shen</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Tantai, Jicheng" sort="Tantai, Jicheng" uniqKey="Tantai J" first="Jicheng" last="Tantai">Jicheng Tantai</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31160576</idno><idno type="pmc">6546683</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6546683</idno><idno type="RBID">PMC:6546683</idno><idno type="doi">10.1038/s41419-019-1660-8</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000059</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000059</idno><idno type="wicri:Area/Pmc/Curation">000059</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000059</idno><idno type="wicri:Area/Pmc/Checkpoint">000649</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000649</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Knockdown of TRIM65 inhibits autophagy and cisplatin resistance in A549/DDP cells by regulating miR-138-5p/ATG7</title><author><name sortKey="Pan, Xufeng" sort="Pan, Xufeng" uniqKey="Pan X" first="Xufeng" last="Pan">Xufeng Pan</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Chen, Yong" sort="Chen, Yong" uniqKey="Chen Y" first="Yong" last="Chen">Yong Chen</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Shen, Yuzhou" sort="Shen, Yuzhou" uniqKey="Shen Y" first="Yuzhou" last="Shen">Yuzhou Shen</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Tantai, Jicheng" sort="Tantai, Jicheng" uniqKey="Tantai J" first="Jicheng" last="Tantai">Jicheng Tantai</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">Cell Death & Disease</title><idno type="eISSN">2041-4889</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 id="Par1">Cisplatin resistance is the main cause of treatment failure in patients with non-small-cell lung cancer (NSCLC). Autophagy is a key mechanism of resistance to chemotherapy. Given that tripartite motif (TRIM)-containing proteins are involved in the regulation of autophagy and chemoresistance, we aimed to study the functions of TRIM protein members in autophagy-mediated chemoresistance of NSCLC. We found that TRIM65 was significantly increased in cisplatin-resistant NSCLC cell line (A549/DDP) as compared to the parental cell line (A549). Knockdown of TRIM65 can enhance cisplatin-induced apoptosis and inhibit autophagy in A549/DDP cells, as indicated by Annexin V/PI staining, caspase3 activity test, and LC3-II immunofluorescence staining. Additionally, knockdown of TRIM65 significantly decreased the expression of an important autophagy mediator, ATG7, which was a potential target of miR-138-5p. miR-138-5p inhibitor significantly abolished the effects of TRIM65 knockdown on autophagy and cisplatin-induced apoptosis. Moreover, TRIM65 induced the ubiquitination and degradation of TNRC6A, resulting in the suppressed expression of miR-138-5p. TRIM65 knockdown inhibited the growth of tumors derived from A549/DDP cells. Furthermore, cisplatin-resistant NSCLC tissues displayed higher expression of TRIM65 mRNA and lower expression of miR-138-5p as compared to cisplatin non-resistant ones. miR-138-5p expression was negatively correlated with TRIM65 mRNA in NSCLC tissues. Collectively, the present study indicates that TRIM65 knockdown attenuates autophagy and cisplatin resistance in A549/DDP cells via regulating miR-138-5p.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Bray, F" uniqKey="Bray F">F Bray</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Howlader, N" uniqKey="Howlader N">N Howlader</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, Mc" uniqKey="Wang M">MC Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kuribayashi, K" uniqKey="Kuribayashi K">K Kuribayashi</name></author><author><name sortKey="Funaguchi, N" uniqKey="Funaguchi N">N Funaguchi</name></author><author><name sortKey="Nakano, T" uniqKey="Nakano T">T Nakano</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Girones, R" uniqKey="Girones R">R Gironés</name></author><author><name sortKey="L Pez, P" uniqKey="L Pez P">P López</name></author><author><name sortKey="Chulvi, R" uniqKey="Chulvi R">R Chulvi</name></author><author><name sortKey="Ca Abate, M" uniqKey="Ca Abate M">M Cañabate</name></author><author><name sortKey="Dolores, T" uniqKey="Dolores T">T Dolores</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chang, A" uniqKey="Chang A">A Chang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mizushima, N" uniqKey="Mizushima N">N Mizushima</name></author><author><name sortKey="Komatsu, M" uniqKey="Komatsu M">M Komatsu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kobayashi, S" uniqKey="Kobayashi S">S Kobayashi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wu, Wk" uniqKey="Wu W">WK Wu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sui, X" uniqKey="Sui X">X Sui</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Aredia, F" uniqKey="Aredia F">F Aredia</name></author><author><name sortKey="Scovassi, Ai" uniqKey="Scovassi A">AI Scovassi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Goldberg, Sb" uniqKey="Goldberg S">SB Goldberg</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lin, S" uniqKey="Lin S">S Lin</name></author><author><name sortKey="Gregory, Ri" uniqKey="Gregory R">RI Gregory</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pink, Rc" uniqKey="Pink R">RC Pink</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xia, L" uniqKey="Xia L">L Xia</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liang, Z" uniqKey="Liang Z">Z Liang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, Q" uniqKey="Wang Q">Q Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Seca, H" uniqKey="Seca H">H Seca</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jin, F" uniqKey="Jin F">F Jin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xu, L" uniqKey="Xu L">L Xu</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Ozato, K" uniqKey="Ozato K">K Ozato</name></author><author><name sortKey="Shin, D M" uniqKey="Shin D">D-M Shin</name></author><author><name sortKey="Chang, T H" uniqKey="Chang T">T-H Chang</name></author><author><name sortKey="Morse, Hc" uniqKey="Morse H">HC Morse</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hatakeyama, S" uniqKey="Hatakeyama S">S Hatakeyama</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hatakeyama, S" uniqKey="Hatakeyama S">S Hatakeyama</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, L" uniqKey="Zhang L">L Zhang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ni, M" uniqKey="Ni M">M Ni</name></author><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y Wang</name></author><author><name sortKey="Xie, L" uniqKey="Xie L">L Xie</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, Y" uniqKey="Liu Y">Y Liu</name></author><author><name sortKey="Zhang, B" uniqKey="Zhang B">B Zhang</name></author><author><name sortKey="Shi, T" uniqKey="Shi T">T Shi</name></author><author><name sortKey="Qin, H" uniqKey="Qin H">H Qin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhao, T T" uniqKey="Zhao T">T-T Zhao</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tan, Z" uniqKey="Tan Z">Z Tan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yu, C" uniqKey="Yu C">C Yu</name></author><author><name sortKey="Chen, S" uniqKey="Chen S">S Chen</name></author><author><name sortKey="Guo, Y" uniqKey="Guo Y">Y Guo</name></author><author><name sortKey="Sun, C" uniqKey="Sun C">C Sun</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Li, S" uniqKey="Li S">S Li</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tanida, I" uniqKey="Tanida I">I Tanida</name></author><author><name sortKey="Ueno, T" uniqKey="Ueno T">T Ueno</name></author><author><name sortKey="Kominami, E" uniqKey="Kominami E">E Kominami</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Qin, X" uniqKey="Qin X">X Qin</name></author><author><name sortKey="Yu, S" uniqKey="Yu S">S Yu</name></author><author><name sortKey="Xu, X" uniqKey="Xu X">X Xu</name></author><author><name sortKey="Shen, B" uniqKey="Shen B">B Shen</name></author><author><name sortKey="Feng, J" uniqKey="Feng J">J Feng</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, Xl" uniqKey="Wang X">XL Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, Zj" uniqKey="Yang Z">ZJ Yang</name></author><author><name sortKey="Chee, Ce" uniqKey="Chee C">CE Chee</name></author><author><name sortKey="Huang, S" uniqKey="Huang S">S Huang</name></author><author><name sortKey="Sinicrope, Fa" uniqKey="Sinicrope F">FA Sinicrope</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, N" uniqKey="Zhang N">N Zhang</name></author><author><name sortKey="Yang, G" uniqKey="Yang G">G Yang</name></author><author><name sortKey="Shao, X" uniqKey="Shao X">X Shao</name></author><author><name sortKey="Wei, L" uniqKey="Wei L">L Wei</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jin, Z" uniqKey="Jin Z">Z Jin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhao, X" uniqKey="Zhao X">X Zhao</name></author><author><name sortKey="Yang, L" uniqKey="Yang L">L Yang</name></author><author><name sortKey="Hu, J" uniqKey="Hu J">J Hu</name></author><author><name sortKey="Ruan, J" uniqKey="Ruan J">J Ruan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tian, S" uniqKey="Tian S">S Tian</name></author><author><name sortKey="Guo, X" uniqKey="Guo X">X Guo</name></author><author><name sortKey="Yu, C" uniqKey="Yu C">C Yu</name></author><author><name sortKey="Sun, C" uniqKey="Sun C">C Sun</name></author><author><name sortKey="Jiang, J" uniqKey="Jiang J">J Jiang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Deng, X S" uniqKey="Deng X">X-S Deng</name></author></analytic></biblStruct></listBibl></div1></back></TEI><pmc article-type="research-article"><pmc-dir>properties 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Cell Death Dis</journal-id><journal-id journal-id-type="iso-abbrev">Cell Death Dis</journal-id><journal-title-group><journal-title>Cell Death & Disease</journal-title></journal-title-group><issn pub-type="epub">2041-4889</issn><publisher><publisher-name>Nature Publishing Group UK</publisher-name><publisher-loc>London</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31160576</article-id><article-id pub-id-type="pmc">6546683</article-id><article-id pub-id-type="publisher-id">1660</article-id><article-id pub-id-type="doi">10.1038/s41419-019-1660-8</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Knockdown of TRIM65 inhibits autophagy and cisplatin resistance in A549/DDP cells by regulating miR-138-5p/ATG7</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Pan</surname><given-names>Xufeng</given-names></name><xref ref-type="aff" rid="Aff1"></xref></contrib><contrib contrib-type="author"><name><surname>Chen</surname><given-names>Yong</given-names></name><xref ref-type="aff" rid="Aff1"></xref></contrib><contrib contrib-type="author"><name><surname>Shen</surname><given-names>Yuzhou</given-names></name><xref ref-type="aff" rid="Aff1"></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Tantai</surname><given-names>Jicheng</given-names></name><address><email>jcttai@163.com</email></address><xref ref-type="aff" rid="Aff1"></xref></contrib><aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 0368 8293</institution-id><institution-id institution-id-type="GRID">grid.16821.3c</institution-id><institution>Department of Thoracic Surgery, Shanghai Chest Hospital,</institution><institution>Shanghai Jiao Tong University,</institution></institution-wrap>Shanghai, China</aff></contrib-group><pub-date pub-type="epub"><day>3</day><month>6</month><year>2019</year></pub-date><pub-date pub-type="pmc-release"><day>3</day><month>6</month><year>2019</year></pub-date><pub-date pub-type="collection"><month>6</month><year>2019</year></pub-date><volume>10</volume><issue>6</issue><elocation-id>429</elocation-id><history><date date-type="received"><day>8</day><month>1</month><year>2019</year></date><date date-type="rev-recd"><day>10</day><month>4</month><year>2019</year></date><date date-type="accepted"><day>30</day><month>4</month><year>2019</year></date></history><permissions><copyright-statement>© The Author(s) 2019</copyright-statement><license license-type="OpenAccess"><license-p><bold>Open Access</bold> This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit <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 id="Abs1"><p id="Par1">Cisplatin resistance is the main cause of treatment failure in patients with non-small-cell lung cancer (NSCLC). Autophagy is a key mechanism of resistance to chemotherapy. Given that tripartite motif (TRIM)-containing proteins are involved in the regulation of autophagy and chemoresistance, we aimed to study the functions of TRIM protein members in autophagy-mediated chemoresistance of NSCLC. We found that TRIM65 was significantly increased in cisplatin-resistant NSCLC cell line (A549/DDP) as compared to the parental cell line (A549). Knockdown of TRIM65 can enhance cisplatin-induced apoptosis and inhibit autophagy in A549/DDP cells, as indicated by Annexin V/PI staining, caspase3 activity test, and LC3-II immunofluorescence staining. Additionally, knockdown of TRIM65 significantly decreased the expression of an important autophagy mediator, ATG7, which was a potential target of miR-138-5p. miR-138-5p inhibitor significantly abolished the effects of TRIM65 knockdown on autophagy and cisplatin-induced apoptosis. Moreover, TRIM65 induced the ubiquitination and degradation of TNRC6A, resulting in the suppressed expression of miR-138-5p. TRIM65 knockdown inhibited the growth of tumors derived from A549/DDP cells. Furthermore, cisplatin-resistant NSCLC tissues displayed higher expression of TRIM65 mRNA and lower expression of miR-138-5p as compared to cisplatin non-resistant ones. miR-138-5p expression was negatively correlated with TRIM65 mRNA in NSCLC tissues. Collectively, the present study indicates that TRIM65 knockdown attenuates autophagy and cisplatin resistance in A549/DDP cells via regulating miR-138-5p.</p></abstract><kwd-group kwd-group-type="npg-subject"><title>Subject terms</title><kwd>Lung cancer</kwd><kwd>Cell biology</kwd></kwd-group><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© The Author(s) 2019</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Chen, Yong" sort="Chen, Yong" uniqKey="Chen Y" first="Yong" last="Chen">Yong Chen</name><name sortKey="Pan, Xufeng" sort="Pan, Xufeng" uniqKey="Pan X" first="Xufeng" last="Pan">Xufeng Pan</name><name sortKey="Shen, Yuzhou" sort="Shen, Yuzhou" uniqKey="Shen Y" first="Yuzhou" last="Shen">Yuzhou Shen</name><name sortKey="Tantai, Jicheng" sort="Tantai, Jicheng" uniqKey="Tantai J" first="Jicheng" last="Tantai">Jicheng Tantai</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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