Research Papers:
Downregulation of miR-101 contributes to epithelial-mesenchymal transition in cisplatin resistance of NSCLC cells by targeting ROCK2
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Abstract
Zhiqiang Ye1,*, Shengli Yin2,*, Zhongzhen Su3, Mingjun Bai4, Haibo Zhang5, Ziqing Hei6, Songwang Cai7
1Department of Emergency, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
2Department of Cardiac Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
3Department of Ultrasonography, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
4Department of Radiology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
5Department of Medical Research Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
6Department of Anesthesiology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
7Department of Cardiothoracic Surgery, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
*These authors have contributed equally to this work
Correspondence to:
Songwang Cai, email: songwangcai#yahoo.com
Ziqing Hei, email: [email protected]
Keywords: miR-101, non-small cell lung cancer, epithelial-mesenchymal transition, chemoresistance, ROCK2
Received: May 29, 2015 Accepted: January 01, 2016 Published: January 09, 2016
ABSTRACT
Chemoresistance and epithelial-mesenchymal transition (EMT) in cancer are linked phenomena. EMT contributes to chemoresistance, however, little is known about whether chemotherapy can induce EMT in cancer cells. Here, we found that miR-101 expression was downregulated in cisplatin-resistant non-small cell lung cancer (NSCLC) cells. Restoration of miR-101 expression inhibited EMT and increased the sensitivity of cisplatin-resistant NSCLC cells to cisplatin in vitro by targeting ROCK2. Furthermore, ROCK2 protein level was inversely correlated with miR-101 level in NSCLC tissue samples. Kaplan-Meier analysis revealed that low miR-101 expression in NSCLC was correlated with poor survival time. In summary, our results provide novel mechanistic insights into the role of miR-101/ROCK2 signaling in the cisplatin resistance of NSCLC cells. Targeting of miR-101 is a potential therapeutic approach for NSCLC.
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