Overexpression of miR-216b sensitizes NSCLC cells to cisplatin-induced apoptosis by targeting c-Jun
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Gang Huang1,*, Jiongwei Pan2,*, Zaiting Ye3,*, Bingmu Fang4, Wei Cheng5 and Zhuo Cao2
1Department of Traditional Chinese Medicine, The Sixth Affiliated Hospital of Wenzhou Medical University, Lishui People’s Hospital, Lishui, 323000, China
2Department of Respiratory, The Sixth Affiliated Hospital of Wenzhou Medical University, Lishui People’s Hospital, Lishui, 323000, China
3Department of Radiology, The Sixth Affiliated Hospital of Wenzhou Medical University, Lishui People’s Hospital, Lishui, China, 323000
4Department of Hematology and Oncology, The Sixth Affiliated Hospital of Wenzhou Medical University, Lishui People’s Hospital, Lishui, 323000, China
5Affiliated Hospital of Xuzhou Medical University, Jiangsu Province Key Laboratory of Anesthesiology and Center for Pain Research and Treatment, Xuzhou, 221000, China
*These authors have contributed equally to this study
Zhuo Cao, email: [email protected]
Wei Cheng, email: [email protected]
Keywords: NSCLC; miR-216b; c-Jun; cisplatin; apoptosis
Received: August 25, 2017 Accepted: September 23, 2017 Published: October 27, 2017
Platinum-based chemotherapy is still be the standard treatment for non-small cell lung cancer (NSCLC). Recently, studies demonstrate that some kinds of microRNAs (miRNAs) are associated with chemosensitivity of NSCLC cells to platinum-based treatment. Unfortunately, cancer cells usually change their expression profile of miRNAs to form drug resistance against chemotherapy. In the present study, we focused on miR-216b to investigate whether miR-216b determined sensitivity of NSCLC cells to cisplatin. We observed that expression level of miR-216b was significantly decreased in NSCLC cell lines when they were under the cisplatin treatment. However, restore of miR-216b by transfecting with its mimics was found to increase the cytotoxicity of cisplatin to NSCLC cells. Studies on mechanisms elucidated that miR-216b targeted c-Jun in NSCLC. Overexpression of miR-216b can suppress the cisplatin-induced upregulation of c-Jun. As the downstream, overexpression of Bcl-xl induced by c-Jun/ATF2 heterodimers was inhibited in miR-216b transfected NSCLC cells. Since Bcl-xl is a key anti-apoptotic protein, we found that sensitivity of NSCLC cells to cisplatin-induced apoptosis was significantly increased because of the overexpression of miR-216b.
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