MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy
Identifieur interne : 000632 ( Main/Merge ); précédent : 000631; suivant : 000633MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy
Auteurs : Ping Liu [République populaire de Chine] ; Chengbin Ma [République populaire de Chine] ; Qiongwei Wu [République populaire de Chine] ; Wenying Zhang [République populaire de Chine] ; Cao Wang [République populaire de Chine] ; Li Yuan [République populaire de Chine] ; Xiaowei Xi [République populaire de Chine]Source :
- Cancer Cell International [ 1475-2867 ] ; 2019.
Abstract
The aim of this study is to examine miRNA profiling and miR-369-3p participates in endometrioid adenocarcinoma (EEC) via the regulation of autophagy.
EEC and its adjacent normal tissues were obtained from 20 clinical patients after surgery. MiRNA profiling was performed using next generation sequencing (NGS) and was validated with quantitative real time PCR (qRT-PCR). qRT-PCR was also employed to measure miR-369-3p and autophagy-related protein 10 (ATG10) expression levels. Western blotting assay was performed to measure the expressions of ATG10 and LC3B. Luciferase reporter assay was conducted to confirm the direct targeting of ATG10 by miR-369-3p. Cell proliferation and migration assays were utilized to analyze the role of miR-369-3p in HEC-1-A cells.
We found that miR-369-3p expression levels were down-regulated in EEC compared to the control tissues. The overexpression of miR-369-3p inhibited cell proliferation and migration in EEC; furthermore, ATG10 expression increased in EEC tissues. ATG10 was found to be a potential target of miR-369-3p via a dual-luciferase reporter assay, and ATG10 was shown to be down-regulated by miR-369-3p in protein levels.
This study revealed that miR-369-3p inhibited cell proliferation and migration by targeting ATG10 via autophagy in EEC.
The online version of this article (10.1186/s12935-019-0897-8) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/s12935-019-0897-8
PubMed: 31337985
PubMed Central: 6624956
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Chine</country><wicri:regionArea>Gynecology Department, Changning Maternity and Infant Health Hospital, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Wu, Qiongwei" sort="Wu, Qiongwei" uniqKey="Wu Q" first="Qiongwei" last="Wu">Qiongwei Wu</name><affiliation wicri:level="1"><nlm:aff id="Aff2">Gynecology Department, Changning Maternity and Infant Health Hospital, Shanghai, 200051 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Gynecology Department, Changning Maternity and Infant Health Hospital, Shanghai</wicri:regionArea><wicri:noRegion>Shanghai</wicri:noRegion></affiliation></author><author><name sortKey="Zhang, Wenying" sort="Zhang, Wenying" uniqKey="Zhang W" first="Wenying" last="Zhang">Wenying Zhang</name><affiliation wicri:level="1"><nlm:aff id="Aff2">Gynecology Department, Changning Maternity and Infant Health Hospital, Shanghai, 200051 China</nlm:aff><country 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institution-id-type="GRID">grid.89957.3a</institution-id><institution>School of Basic Medical Sciences of Nanjing Medical University,</institution></institution-wrap>Nanjing, 211166 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Nanjing</wicri:regionArea></affiliation></author><author><name sortKey="Xi, Xiaowei" sort="Xi, Xiaowei" uniqKey="Xi X" first="Xiaowei" last="Xi">Xiaowei Xi</name><affiliation wicri:level="1"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1760 4628</institution-id><institution-id institution-id-type="GRID">grid.412478.c</institution-id><institution>Gynecology Department,</institution><institution>Shanghai General Hospital of Nanjing Medical University,</institution></institution-wrap>Shanghai, 200080 China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Shanghai</wicri:regionArea></affiliation></author></analytic><series><title level="j">Cancer Cell International</title><idno type="eISSN">1475-2867</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p id="Par1">The aim of this study is to examine miRNA profiling and miR-369-3p participates in endometrioid adenocarcinoma (EEC) via the regulation of autophagy.</p></sec><sec><title>Methods</title><p id="Par2">EEC and its adjacent normal tissues were obtained from 20 clinical patients after surgery. MiRNA profiling was performed using next generation sequencing (NGS) and was validated with quantitative real time PCR (qRT-PCR). qRT-PCR was also employed to measure miR-369-3p and autophagy-related protein 10 (ATG10) expression levels. Western blotting assay was performed to measure the expressions of ATG10 and LC3B. Luciferase reporter assay was conducted to confirm the direct targeting of ATG10 by miR-369-3p. Cell proliferation and migration assays were utilized to analyze the role of miR-369-3p in HEC-1-A cells.</p></sec><sec><title>Results</title><p id="Par3">We found that miR-369-3p expression levels were down-regulated in EEC compared to the control tissues. The overexpression of miR-369-3p inhibited cell proliferation and migration in EEC; furthermore, ATG10 expression increased in EEC tissues. ATG10 was found to be a potential target of miR-369-3p via a dual-luciferase reporter assay, and ATG10 was shown to be down-regulated by miR-369-3p in protein levels.</p></sec><sec><title>Conclusions</title><p id="Par4">This study revealed that miR-369-3p inhibited cell proliferation and migration by targeting ATG10 via autophagy in EEC.</p></sec><sec><title>Electronic supplementary material</title><p>The online version of this article (10.1186/s12935-019-0897-8) contains supplementary material, which is available to authorized users.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Jemal, A" uniqKey="Jemal A">A Jemal</name></author><author><name sortKey="Siegel, R" uniqKey="Siegel R">R Siegel</name></author><author><name sortKey="Ward, E" uniqKey="Ward E">E Ward</name></author><author><name sortKey="Hao, Y" uniqKey="Hao Y">Y Hao</name></author><author><name sortKey="Xu, J" uniqKey="Xu J">J Xu</name></author><author><name 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