Oncotarget

Research Papers:

MicroRNA-520g promotes epithelial ovarian cancer progression and chemoresistance via DAPK2 repression

Jing Zhang, Lei Liu, Yunyan Sun, Jiandong Xiang, Dongmei Zhou, Li Wang, Huali Xu, Xiaoming Yang, Na Du, Meng Zhang, Qin Yan and Xiaowei Xi _

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Oncotarget. 2016; 7:26516-26534. https://doi.org/10.18632/oncotarget.8530

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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: [email protected]

Qin Yan, e-mail: [email protected]

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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