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OIP5-AS1/miR-137/ZNF217 Axis Promotes Malignant Behaviors in Epithelial Ovarian Cancer

Authors Guo L, Chen J, Liu D, Liu L

Received 7 November 2019

Accepted for publication 8 June 2020

Published 3 August 2020 Volume 2020:12 Pages 6707—6717

DOI https://doi.org/10.2147/CMAR.S237726

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr Antonella D'Anneo


Linlin Guo, Jiabao Chen, Dong Liu, Lili Liu

Department of Obstetrics and Gynecology, First Affiliated Hospital of Jinzhou Medical University, Jinnzhou, Liaoning, People’s Republic of China

Correspondence: Lili Liu
Department of Obstetrics and Gynecology, First Affiliated Hospital of Jinzhou Medical University, No. 2, Section 5, Renming Street, Jinnzhou, Liaoning, People’s Republic of China
Email liuao981075@163.com

Background: Long non-coding RNAs (lncRNAs) have been reported to play crucial regulatory roles in cellular activities and are associated with the carcinogenesis of various diseases. OIP5-AS1, as a novel lncRNA, function in epithelial ovarian cancer (EOC) still remains unclear.
Material and Methods: qRT-PCR and Western blot analyses were performed to measure relevant expression, as needed. A series of functional experiments were performed to determine the role of OIP5-AS1 in EOC cells. Luciferase report, RNA pull down and RIP assays were performed to testify the interaction between relevant RNAs.
Results: We found that OIP5-AS1 was significantly overexpressed in EOC. Knockdown of OIP5-AS1 inhibited cell proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) process, yet facilitated apoptosis in vitro. OIP5-AS1 functioned as a competing endogenous RNA (ceRNA) to elevate ZNF217 expression through sponging miR-137. Furthermore, miR-137 inhibition and ZNF217 upregulation can reverse the effects of silencing OIP5-AS1 on the cellular activities of ovarian cancer cells. Also, depleted OIP5-AS1 hindered tumor growth and metastasis in vivo.
Conclusion: OIP5-AS1 regulated ovarian cancer progression via modulating miR-137/ZNF217 signaling, suggesting that targeting OIP5-AS1 could be conducive to EOC clinical treatment.

Keywords: OIP5-AS1, miR-137, ZNF217, epithelial ovarian cancer

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