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NEAT1 regulates cell proliferation and apoptosis of ovarian cancer by miR-34a-5p/BCL2

Authors Ding N, Wu H, Tao T, Peng E

Received 23 May 2017

Accepted for publication 28 July 2017

Published 6 October 2017 Volume 2017:10 Pages 4905—4915


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 2

Editor who approved publication: Dr XuYu Yang

Nan Ding,1 Haiying Wu,1 Tao Tao,1 Erxuan Peng2

1Department of Obstetrics and Gynecology, Henan Provincial People’s Hospital, 2Department of Obstetrics and Gynecology, Henan Provincial Tumor Hospital, Zhengzhou, China

Background: Nuclear enriched abundant transcript 1 (NEAT1) has been demonstrated to act as a tumor inhibitor in many cancers. However, the role of NEAT1 in the development of ovarian cancer (OC) remains far from being elaborated. Hence, the aim of this study is to investigate the expression and function of NEAT1 in OC.
Materials and methods: The expression level of NEAT1 was determined by quantitative real-time polymerase chain reaction in OC cell lines. MTT assay, caspase-3 activity assay, and flow cytometry analysis were conducted to investigate the effects of NEAT1, miR-34a-5p, or B-cell lymphoma-2 (BCL2) on OC cell proliferation and apoptosis. Luciferase reporter assay was used to confirm the interaction of NEAT1, BCL2, and miR-34a-5p in OC cells.
Results: NEAT1 was significantly upregulated in OC cell lines. NEAT1 overexpression promoted proliferation by increasing the proportion of cells in S phase and suppressed apoptosis of OC cells, while knockdown of NEAT1 had the opposite effect. In addition, NEAT1 was demonstrated to directly interact with miR-34a-5p and exert its oncogenic role in OC by negatively regulating miR-34a-5p. Moreover, miR-34a-5p could directly target BCL2 and suppressed its expression. miR-34a-5p overexpression suppressed OC cell proliferation and triggered apoptosis by targeting BCL2. Furthermore, NEAT1 knockdown suppressed BCL2 expression, while anti-miR-34a-5p dramatically abated the inhibitory effect of si-NEAT1 on BCL2 expression.
Conclusion: NEAT1 regulated proliferation and apoptosis of OC cells by miR-34a-5p/BCL2, providing a potential therapeutic approach for the treatment of OC patients.

NEAT1, miR-34a-5p, BCL2, ovarian cancer, caspase-3, ceRNA

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