Long non-coding RNA GBCDRlnc1 induces chemoresistance of gallbladder cancer cells by activating autophagy
Identifieur interne : 000682 ( Main/Exploration ); précédent : 000681; suivant : 000683Long non-coding RNA GBCDRlnc1 induces chemoresistance of gallbladder cancer cells by activating autophagy
Auteurs : Qiang Cai [République populaire de Chine] ; Shouhua Wang [République populaire de Chine] ; Longyang Jin [République populaire de Chine] ; Mingzhe Weng [République populaire de Chine] ; Di Zhou [République populaire de Chine] ; Jiandong Wang [République populaire de Chine] ; Zhaohui Tang [République populaire de Chine] ; Zhiwei Quan [République populaire de Chine]Source :
- Molecular Cancer [ 1476-4598 ] ; 2019.
Abstract
Gallbladder cancer is the most common biliary tract malignancy and not sensitive to chemotherapy. Autophagy is an important factor prolonging the survival of cancer cells under chemotherapeutic stress. We aimed to investigate the role of long non-coding RNAs (lncRNAs) in autophagy and chemoresistance of gallbladder cancer cells.
We established doxorubicin (Dox)-resistant gallbladder cancer cells and used microarray analysis to compare the expression profiles of lncRNAs in Dox-resistant gallbladder cancer cells and their parental cells. Knockdown or exogenous expression of lncRNA combined with in vitro and in vivo assays were performed to prove the functional significance of lncRNA. The effects of lncRNA on autophagy were assessed by stubRFP-sensGFP-LC3 and western blot. We used RNA pull-down and mass spectrometry analysis to identify the target proteins of lncRNA.
The drug-resistant property of gallbladder cancer cells is related to their enhanced autophagic activity. And we found a lncRNA ENST00000425894 termed gallbladder cancer drug resistance-associated lncRNA1 (GBCDRlnc1) that serves as a critical regulator in gallbladder cancer chemoresistance. Furthermore, we discovered that GBCDRlnc1 is upregulated in gallbladder cancer tissues. Knockdown of GBCDRlnc1, via inhibiting autophagy at initial stage, enhanced the sensitivity of Dox-resistant gallbladder cancer cells to Dox in vitro and in vivo. Mechanically, we identified that GBCDRlnc1 interacts with phosphoglycerate kinase 1 and inhibits its ubiquitination in Dox-resistant gallbladder cancer cells, which leads to the down-regulation of autophagy initiator ATG5-ATG12 conjugate.
Our findings established that the chemoresistant driver GBCDRlnc1 might be a candidate therapeutic target for the treatment of advanced gallbladder cancer.
The online version of this article (10.1186/s12943-019-1016-0) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/s12943-019-1016-0
PubMed: 30953511
PubMed Central: 6449938
Affiliations:
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Chine</country><wicri:regionArea>Shanghai</wicri:regionArea></affiliation></author></analytic><series><title level="j">Molecular Cancer</title><idno type="eISSN">1476-4598</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">Gallbladder cancer is the most common biliary tract malignancy and not sensitive to chemotherapy. Autophagy is an important factor prolonging the survival of cancer cells under chemotherapeutic stress. We aimed to investigate the role of long non-coding RNAs (lncRNAs) in autophagy and chemoresistance of gallbladder cancer cells.</p></sec><sec><title>Methods</title><p id="Par2">We established doxorubicin (Dox)-resistant gallbladder cancer cells and used microarray analysis to compare the expression profiles of lncRNAs in Dox-resistant gallbladder cancer cells and their parental cells. Knockdown or exogenous expression of lncRNA combined with in vitro and in vivo assays were performed to prove the functional significance of lncRNA. The effects of lncRNA on autophagy were assessed by stubRFP-sensGFP-LC3 and western blot. We used RNA pull-down and mass spectrometry analysis to identify the target proteins of lncRNA.</p></sec><sec><title>Results</title><p id="Par3">The drug-resistant property of gallbladder cancer cells is related to their enhanced autophagic activity. And we found a lncRNA ENST00000425894 termed gallbladder cancer drug resistance-associated lncRNA1 (GBCDRlnc1) that serves as a critical regulator in gallbladder cancer chemoresistance. Furthermore, we discovered that GBCDRlnc1 is upregulated in gallbladder cancer tissues. Knockdown of GBCDRlnc1, via inhibiting autophagy at initial stage, enhanced the sensitivity of Dox-resistant gallbladder cancer cells to Dox in vitro and in vivo. Mechanically, we identified that GBCDRlnc1 interacts with phosphoglycerate kinase 1 and inhibits its ubiquitination in Dox-resistant gallbladder cancer cells, which leads to the down-regulation of autophagy initiator ATG5-ATG12 conjugate.</p></sec><sec><title>Conclusions</title><p id="Par4">Our findings established that the chemoresistant driver GBCDRlnc1 might be a candidate therapeutic target for the treatment of advanced gallbladder cancer.</p></sec><sec><title>Electronic supplementary material</title><p>The online version of this article (10.1186/s12943-019-1016-0) contains supplementary material, which is available to authorized users.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Misra, S" uniqKey="Misra S">S Misra</name></author><author><name sortKey="Chaturvedi, A" uniqKey="Chaturvedi A">A Chaturvedi</name></author><author><name sortKey="Misra, Nc" uniqKey="Misra N">NC Misra</name></author><author><name 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uniqKey="Yu J">J Yu</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Cai, Qiang" sort="Cai, Qiang" uniqKey="Cai Q" first="Qiang" last="Cai">Qiang Cai</name></noRegion><name sortKey="Cai, Qiang" sort="Cai, Qiang" uniqKey="Cai Q" first="Qiang" last="Cai">Qiang Cai</name><name sortKey="Jin, Longyang" sort="Jin, Longyang" uniqKey="Jin L" first="Longyang" last="Jin">Longyang Jin</name><name sortKey="Quan, Zhiwei" sort="Quan, Zhiwei" uniqKey="Quan Z" first="Zhiwei" last="Quan">Zhiwei Quan</name><name sortKey="Tang, Zhaohui" sort="Tang, Zhaohui" uniqKey="Tang Z" first="Zhaohui" last="Tang">Zhaohui Tang</name><name sortKey="Wang, Jiandong" sort="Wang, Jiandong" uniqKey="Wang J" first="Jiandong" last="Wang">Jiandong Wang</name><name sortKey="Wang, Shouhua" sort="Wang, Shouhua" uniqKey="Wang S" first="Shouhua" last="Wang">Shouhua Wang</name><name sortKey="Weng, Mingzhe" sort="Weng, Mingzhe" uniqKey="Weng M" first="Mingzhe" last="Weng">Mingzhe Weng</name><name sortKey="Zhou, Di" sort="Zhou, Di" uniqKey="Zhou D" first="Di" last="Zhou">Di Zhou</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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