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miR-31-5p Regulates 14-3-3 ɛ to Inhibit Prostate Cancer 22RV1 Cell Survival and Proliferation via PI3K/AKT/Bcl-2 Signaling Pathway

Authors Zhao J, Xu H, Duan Z, Chen X, Ao Z, Chen Y, Ruan Y, Ni M

Received 30 January 2020

Accepted for publication 3 July 2020

Published 31 July 2020 Volume 2020:12 Pages 6679—6694

DOI https://doi.org/10.2147/CMAR.S247780

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 4

Editor who approved publication: Dr Sanjeev Srivastava


Jiafu Zhao,1– 3 Houqiang Xu,1– 3 Zhiqiang Duan,2,3 Xiang Chen,2,3 Zheng Ao,2,3 Yinglian Chen,2,3 Yong Ruan,2,3 Mengmeng Ni2,3

1College of Life Science, Guizhou University, Guiyang 550025, People’s Republic of China; 2Key Laboratory of Animal Genetics, Breeding and Reproduction in the Plateau Mountainous Region, Ministry of Education, Guizhou University, Guiyang 550025, People’s Republic of China; 3College of Animal Science, Guizhou University, Guiyang 550025, People’s Republic of China

Correspondence: Houqiang Xu
College of Life Science, Guizhou University, No. 197, Huashi Road, Huaxi District, Guiyang City, Guizhou Province, People’s Republic of China
Tel +86 13765056884
Fax +86 851 88298005
Email gzdxxhq@163.com

Introduction: Prostate cancer (PCa) is one of the most common malignancies, and almost all patients with advanced PCa will develop castration-resistant prostate cancer (CRPC) after receiving endocrine therapy. Effective treatment for patients with CRPC has not been established. Novel approaches are needed to identify therapeutic targets for CRPC.
Purpose: Recent research studies have found that members of the 14-3-3 family play an important role in the development and progression of PCa. Previous results have shown that 14-3-3 ɛ is significantly upregulated in several cancers. This study aimed to identify novel miRNAs that regulate 14-3-3 ɛ expression and therapeutic targets for CRPC.
Methods: In this study, we used computation and experimental approaches for the prediction and verification of the miRNAs targeting 14-3-3 ɛ, and investigated the potential roles of 14-3-3 ɛ in the survival and proliferation of 22RV1 cells.
Results: We confirm that mir-31-5p is downregulated in 22RV1 cells and acts as a tumor suppressor by regulating 14-3-3 ɛ. Ectopic expression of miR-31-5p or 14-3-3 ɛ interference significantly inhibits cell proliferation, invasion, and migration in 22RV1 cells, as well as promotes cell apoptosis via the PI3K/AKT/Bcl-2 signaling pathway. Moreover, 14-3-3 ɛ is required for the miR-31-5p-mediated upregulation of the PI3K/AKT/Bcl-2 signaling pathway.
Conclusion: Our findings provide information on the underlying mechanisms of miR-31-5p/ 14-3-3 ɛ in 22RV1 cell proliferation and apoptosis through the PI3K/AKT/Bcl-2 signaling pathway. These results suggest that miR-31-5p and 14-3-3 ɛ may potentially be utilized as novel prognostic markers and therapeutic targets for PCa treatment.

Keywords: prostate cancer, miR-31-5p, 14-3-3 ϵ, PI3K/AKT/Bcl-2 pathway, cell proliferation, cell apoptosis

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