miR-31-5p Regulates 14-3-3 ɛ to Inhibit Prostate Cancer 22RV1 Cell Survival and Proliferation via PI3K/AKT/Bcl-2 Signaling Pathway
Received 30 January 2020
Accepted for publication 3 July 2020
Published 31 July 2020 Volume 2020:12 Pages 6679—6694
Checked for plagiarism Yes
Review by Single-blind
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
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
This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.Download Article [PDF] View Full Text [HTML][Machine readable]