Research Papers:
MicroRNA-520g promotes epithelial ovarian cancer progression and chemoresistance via DAPK2 repression
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Abstract
Jing Zhang1,*, Lei Liu2,*, Yunyan Sun1, Jiandong Xiang1, Dongmei Zhou1, Li Wang1, Huali Xu1, Xiaoming Yang1, Na Du1, Meng Zhang3, Qin Yan1, Xiaowei Xi1
1Department of Obstetrics and Gynecology, Shanghai Jiao Tong University Affiliated First People’s Hospital, Shanghai, China
2Department of Obstetrics and Gynecology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
3Department of Pathology, Fudan University Affiliated Shanghai Cancer Center, Shanghai, China
*These authors contributed equally to this work
Correspondence to:
Xiaowei Xi, e-mail: xixiaowei1966@126.com
Qin Yan, e-mail: yanqin76@126.com
Keywords: miR-520g, epithelial ovarian cancer, progression, chemoresistance, DAPK2
Received: June 17, 2015 Accepted: February 18, 2016 Published: April 01, 2016
ABSTRACT
The lack of efficient tumor progression and chemoresistance indicators leads to high mortality in epithelial ovarian cancer (EOC) patients. Dysregulated miR-520g expression is involved in these processes in hepatic and colorectal cancers. In this study, we found that miR-520g expression gradually increased across normal, benign, borderline and EOC tissues. High miR-520g expression promoted tumor progression and chemoresistance to platinum-based chemotherapy, and reduced survival in EOC patients. miR-520g upregulation increased EOC cell proliferation, induced cell cycle transition and promoted cell invasion, while miR-520g downregulation inhibited tumor-related functions. In vivo, overexpression or downregulation of miR-520g respectively generated larger or smaller subcutaneous xenografts in nude mice. Death-associated protein kinase 2 (DAPK2) was a direct target of miR-520g. In 116 EOC tissue samples, miR-520g expression was significantly lower following DAPK2 overexpression. DAPK2 overexpression or miR-520g knockdown reduced EOC cell proliferation, invasion, wound healing and chemoresistance. This study suggests that miR-520g contributes to tumor progression and drug resistance by post-transcriptionally downregulating DAPK2, and that miR-520g may be a valuable therapeutic target in patients with EOC.

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