miR-106a Regulates Cell Proliferation and Autophagy by Targeting LKB1 in HPV-16-Associated Cervical Cancer.
Identifieur interne : 000004 ( Main/Exploration ); précédent : 000003; suivant : 000005miR-106a Regulates Cell Proliferation and Autophagy by Targeting LKB1 in HPV-16-Associated Cervical Cancer.
Auteurs : Xiujie Cui [République populaire de Chine] ; Xiao Wang [République populaire de Chine] ; Xiaoqing Zhou [République populaire de Chine] ; Jihui Jia [République populaire de Chine] ; Hanxiang Chen [République populaire de Chine] ; Weiming ZhaoSource :
- Molecular cancer research : MCR [ 1557-3125 ] ; 2020.
Abstract
miR-106a is aberrantly regulated in various tumors and plays an important role in carcinogenesis. However, the biological role and molecular mechanism by which miR-106a contributes to cervical squamous cell carcinoma (CSCC) remains elusive. In this study, we verified that miR-106a was elevated in both human papilloma virus (HPV) 16-positive CSCC tissues and cell lines. ROC curve analysis showed that miR-106a could well distinguish HPV-16-positive CSCC tissues from normal cervical squamous epithelium tissues. High expression of miR-106a was associated with malignant clinicopathologic parameters in CSCC tissues. Exogenous expression of miR-106a greatly promoted cervical cancer cell proliferation while attenuated autophagy. Furthermore, a novel target of miR-106a, liver kinase B1 (LKB1), a proven tumor suppressor in cervical cancer was verified. Here we confirmed LKB1 was negatively correlated with malignant clinicopathologic parameters in CSCC tissues. Overexpression of LKB1 neutralized the effect of miR-106a on proliferation and autophagy in cervical cancer cell lines. In addition, the role of miR-106a in cell proliferation and autophagy was via LKB1 and its downstream pathway AMP-activated protein kinase-mammalian target of rapamycin. Of note, miR-106a was upregulated by HPV-16 E7 protein. The function of HPV-16 E7 to cell proliferation was suppressed when knockdown miR-106a in HPV-16 E7-expressing cells. IMPLICATIONS: Our study highlights the tumorigenic role and regulatory mechanism of miR-106a in CSCC. miR-106a may be a potential therapeutic target in HPV-associated cervical cancer.
DOI: 10.1158/1541-7786.MCR-19-1114
PubMed: 32345599
Affiliations:
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China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong</wicri:regionArea><wicri:noRegion>Shandong</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Xiao" sort="Wang, Xiao" uniqKey="Wang X" first="Xiao" last="Wang">Xiao Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong</wicri:regionArea><wicri:noRegion>Shandong</wicri:noRegion></affiliation></author><author><name sortKey="Zhou, Xiaoqing" sort="Zhou, Xiaoqing" uniqKey="Zhou X" first="Xiaoqing" last="Zhou">Xiaoqing Zhou</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong</wicri:regionArea><wicri:noRegion>Shandong</wicri:noRegion></affiliation></author><author><name sortKey="Jia, Jihui" sort="Jia, Jihui" uniqKey="Jia J" first="Jihui" last="Jia">Jihui Jia</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong</wicri:regionArea><wicri:noRegion>Shandong</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Hanxiang" sort="Chen, Hanxiang" uniqKey="Chen H" first="Hanxiang" last="Chen">Hanxiang Chen</name><affiliation><nlm:affiliation>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, P.R. China. zhaowm@sdu.edu.cn okayhensen@163.com.</nlm:affiliation><wicri:noCountry code="subField">P.R.</wicri:noCountry></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Laboratory, Shandong Provincial Qianfoshan Hospital, The First Affiliated Hospital of Shandong First Medical University, Jinan, Shandong, P.R. China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Shandong Provincial Qianfoshan Hospital, The First Affiliated Hospital of Shandong First Medical University, Jinan, Shandong</wicri:regionArea><wicri:noRegion>Shandong</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Weiming" sort="Zhao, Weiming" uniqKey="Zhao W" first="Weiming" last="Zhao">Weiming Zhao</name><affiliation><nlm:affiliation>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, P.R. China. zhaowm@sdu.edu.cn okayhensen@163.com.</nlm:affiliation><wicri:noCountry code="subField">P.R.</wicri:noCountry></affiliation></author></analytic><series><title level="j">Molecular cancer research : MCR</title><idno type="eISSN">1557-3125</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">miR-106a is aberrantly regulated in various tumors and plays an important role in carcinogenesis. However, the biological role and molecular mechanism by which miR-106a contributes to cervical squamous cell carcinoma (CSCC) remains elusive. In this study, we verified that miR-106a was elevated in both human papilloma virus (HPV) 16-positive CSCC tissues and cell lines. ROC curve analysis showed that miR-106a could well distinguish HPV-16-positive CSCC tissues from normal cervical squamous epithelium tissues. High expression of miR-106a was associated with malignant clinicopathologic parameters in CSCC tissues. Exogenous expression of miR-106a greatly promoted cervical cancer cell proliferation while attenuated autophagy. Furthermore, a novel target of miR-106a, liver kinase B1 (LKB1), a proven tumor suppressor in cervical cancer was verified. Here we confirmed LKB1 was negatively correlated with malignant clinicopathologic parameters in CSCC tissues. Overexpression of LKB1 neutralized the effect of miR-106a on proliferation and autophagy in cervical cancer cell lines. In addition, the role of miR-106a in cell proliferation and autophagy was via LKB1 and its downstream pathway AMP-activated protein kinase-mammalian target of rapamycin. Of note, miR-106a was upregulated by HPV-16 E7 protein. The function of HPV-16 E7 to cell proliferation was suppressed when knockdown miR-106a in HPV-16 E7-expressing cells. IMPLICATIONS: Our study highlights the tumorigenic role and regulatory mechanism of miR-106a in CSCC. miR-106a may be a potential therapeutic target in HPV-associated cervical cancer.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32345599</PMID><DateRevised><Year>2020</Year><Month>11</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1557-3125</ISSN><JournalIssue CitedMedium="Internet"><Volume>18</Volume><Issue>8</Issue><PubDate><Year>2020</Year><Month>08</Month></PubDate></JournalIssue><Title>Molecular cancer research : MCR</Title><ISOAbbreviation>Mol Cancer Res</ISOAbbreviation></Journal><ArticleTitle>miR-106a Regulates Cell Proliferation and Autophagy by Targeting LKB1 in HPV-16-Associated Cervical Cancer.</ArticleTitle><Pagination><MedlinePgn>1129-1141</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1158/1541-7786.MCR-19-1114</ELocationID><Abstract><AbstractText>miR-106a is aberrantly regulated in various tumors and plays an important role in carcinogenesis. However, the biological role and molecular mechanism by which miR-106a contributes to cervical squamous cell carcinoma (CSCC) remains elusive. In this study, we verified that miR-106a was elevated in both human papilloma virus (HPV) 16-positive CSCC tissues and cell lines. ROC curve analysis showed that miR-106a could well distinguish HPV-16-positive CSCC tissues from normal cervical squamous epithelium tissues. High expression of miR-106a was associated with malignant clinicopathologic parameters in CSCC tissues. Exogenous expression of miR-106a greatly promoted cervical cancer cell proliferation while attenuated autophagy. Furthermore, a novel target of miR-106a, liver kinase B1 (LKB1), a proven tumor suppressor in cervical cancer was verified. Here we confirmed LKB1 was negatively correlated with malignant clinicopathologic parameters in CSCC tissues. Overexpression of LKB1 neutralized the effect of miR-106a on proliferation and autophagy in cervical cancer cell lines. In addition, the role of miR-106a in cell proliferation and autophagy was via LKB1 and its downstream pathway AMP-activated protein kinase-mammalian target of rapamycin. Of note, miR-106a was upregulated by HPV-16 E7 protein. The function of HPV-16 E7 to cell proliferation was suppressed when knockdown miR-106a in HPV-16 E7-expressing cells. IMPLICATIONS: Our study highlights the tumorigenic role and regulatory mechanism of miR-106a in CSCC. miR-106a may be a potential therapeutic target in HPV-associated cervical cancer.</AbstractText><CopyrightInformation>©2020 American Association for Cancer Research.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cui</LastName><ForeName>Xiujie</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Xiao</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Pathology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhou</LastName><ForeName>Xiaoqing</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jia</LastName><ForeName>Jihui</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Chen</LastName><ForeName>Hanxiang</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, P.R. China. zhaowm@sdu.edu.cn okayhensen@163.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Clinical Laboratory, Shandong Provincial Qianfoshan Hospital, The First Affiliated Hospital of Shandong First Medical University, Jinan, Shandong, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y" EqualContrib="Y"><LastName>Zhao</LastName><ForeName>Weiming</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, P.R. China. zhaowm@sdu.edu.cn okayhensen@163.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>04</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Cancer Res</MedlineTA><NlmUniqueID>101150042</NlmUniqueID><ISSNLinking>1541-7786</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>11</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>03</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>04</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>4</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>4</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>4</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32345599</ArticleId><ArticleId IdType="pii">1541-7786.MCR-19-1114</ArticleId><ArticleId IdType="doi">10.1158/1541-7786.MCR-19-1114</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><noCountry><name sortKey="Zhao, Weiming" sort="Zhao, Weiming" uniqKey="Zhao W" first="Weiming" last="Zhao">Weiming Zhao</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Cui, Xiujie" sort="Cui, Xiujie" uniqKey="Cui X" first="Xiujie" last="Cui">Xiujie Cui</name></noRegion><name sortKey="Chen, Hanxiang" sort="Chen, Hanxiang" uniqKey="Chen H" first="Hanxiang" last="Chen">Hanxiang Chen</name><name sortKey="Jia, Jihui" sort="Jia, Jihui" uniqKey="Jia J" first="Jihui" last="Jia">Jihui Jia</name><name sortKey="Wang, Xiao" sort="Wang, Xiao" uniqKey="Wang X" first="Xiao" last="Wang">Xiao Wang</name><name sortKey="Zhou, Xiaoqing" sort="Zhou, Xiaoqing" uniqKey="Zhou X" first="Xiaoqing" last="Zhou">Xiaoqing Zhou</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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