The long non-coding RNA ANRIL promotes proliferation and cell cycle progression and inhibits apoptosis and senescence in epithelial ovarian cancer
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Jun-jun Qiu1,2,3, Yan Wang4,5, Ying-lei Liu6, Ying Zhang1,2,3, Jing-xin Ding1,2,3, Ke-qin Hua1,2,3
1Department of Gynecology, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China
2Department of Obstetrics and Gynecology of Shanghai Medical College, Fudan University, Shanghai, China
3Shanghai Key Laboratory of Female Reproductive Endocrine-Related Diseases, Fudan University, Shanghai, China
4Cancer Institute, Shanghai Medical College, Fudan University, Shanghai, China
5Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China
6Department of Gynecology, The Second Affiliated Hospital of Nantong University, Nantong, China
Ke-qin Hua, email: firstname.lastname@example.org
Keywords: ANRIL, proliferation, cell cycle, apoptosis, senescence
Received: September 03, 2015 Accepted: February 16, 2016 Published: April 15, 2016
Antisense non-coding RNA in the INK4 locus (ANRIL) has been implicated in a variety of cancers. In the present study, we evaluated ANRIL expression in epithelial ovarian cancer (EOC) and defined its clinical implications and biological functions. ANRIL was overexpressed in EOC tissues relative to normal controls. Overexpression correlated with advanced International Federation of Gynecologists and Obstetricians stage and high histological grade. Multivariate analysis indicated that ANRIL is an independent prognostic factor for overall survival in EOC. Gain- and loss-of-function experiments demonstrated that ANRIL promotes EOC cell proliferation both in vitro and in vivo. The proliferative effect was linked to the promotion of cell cycle progression and inhibition of apoptosis and senescence. Down-regulation of P15INK4B and up-regulation of Bcl-2 by ANRIL may partially explain ANRIL-induced EOC cell proliferation. This study is the first to establish that ANRIL promotes EOC progression and is a potential prognostic biomarker.
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