Downregulation of miR-101 contributes to epithelial-mesenchymal transition in cisplatin resistance of NSCLC cells by targeting ROCK2

// Zhiqiang Ye 1, * , Shengli Yin 2, * , Zhongzhen Su 3 , Mingjun Bai 4 , Haibo Zhang 5 , Ziqing Hei 6 , Songwang Cai 7 1 Department of Emergency, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China 2 Department of Cardiac Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China 3 Department of Ultrasonography, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China 4 Department of Radiology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China 5 Department of Medical Research Center, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China 6 Department of Anesthesiology, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China 7 Department 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: heiziqing@sina.com 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.