Abstract

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.

Highlights

  • Epithelial ovarian cancer (EOC) is one of the most aggressive malignancies [1,2,3]

  • We showed that Antisense non‐coding RNA in the INK4 locus (ANRIL) expression was significantly elevated in 102 EOC tissues compared with 30 noncancerous tissues using Quantitative real‐time polymerase chain reaction (qRT‐PCR) (P < 0.01; Figure 1A)

  • These results suggested that ANRIL overexpression was associated with a more malignant ovarian cancer phenotype

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Summary

Introduction

Epithelial ovarian cancer (EOC) is one of the most aggressive malignancies [1,2,3]. The prognosis of EOC is very poor, primarily because it is typically diagnosed at an advanced stage and because of the lack of efficacious therapies [3]. A better understanding of the molecular mechanisms involved in EOC progression may facilitate the identification of novel markers and effective therapeutic strategies that can prolong survival and improve patient outcomes. Mounting evidence indicates that the molecular mechanisms of carcinogenesis and cancer progression involve to protein‐coding genes, and non‐coding RNAs. Long non‐coding RNAs (lncRNAs, > 200 nucleotides) were initially thought to be the “dark matter” of the genome but have recently emerged as critical components of the cancer transcriptome [6, 7]. Many lncRNAs control carcinogenesis and cancer progression, and potentially represent a new avenue for cancer research [8,9,10,11,12,13,14,15,16,17]. Elucidation of the roles of these lncRNAs will provide insight into the molecular biology underlying cancer initiation and progression

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