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微小RNA-31-5p通过PI3K/AKT/Bcl-2信号通路发挥调控作用以抑制前列腺癌22RV1细胞的存活和增殖。

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

作者信息

Zhao Jiafu, Xu Houqiang, Duan Zhiqiang, Chen Xiang, Ao Zheng, Chen Yinglian, Ruan Yong, Ni Mengmeng

机构信息

College of Life Science, Guizhou University, Guiyang 550025, People's Republic of China.

Key Laboratory of Animal Genetics, Breeding and Reproduction in the Plateau Mountainous Region, Ministry of Education, Guizhou University, Guiyang 550025, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Jul 31;12:6679-6694. doi: 10.2147/CMAR.S247780. eCollection 2020.

DOI:10.2147/CMAR.S247780
PMID:32801901
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7402864/
Abstract

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 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 . Ectopic expression of miR-31-5p or 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, 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/ 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.

摘要

引言

前列腺癌(PCa)是最常见的恶性肿瘤之一,几乎所有晚期PCa患者在接受内分泌治疗后都会发展为去势抵抗性前列腺癌(CRPC)。目前尚未确立针对CRPC患者的有效治疗方法。需要新的方法来确定CRPC的治疗靶点。

目的

最近的研究发现,14-3-3家族成员在PCa的发生和发展中起重要作用。先前的结果表明, 在几种癌症中显著上调。本研究旨在鉴定调节14-3-3ε表达的新型miRNA以及CRPC的治疗靶点。

方法

在本研究中,我们使用计算和实验方法来预测和验证靶向14-3-3ε的miRNA,并研究14-3-3ε在22RV1细胞存活和增殖中的潜在作用。

结果

我们证实mir-31-5p在22RV1细胞中表达下调,并通过调节 发挥肿瘤抑制作用。miR-31-5p的异位表达或 干扰显著抑制22RV1细胞的增殖、侵袭和迁移,并通过PI3K/AKT/Bcl-2信号通路促进细胞凋亡。此外, 是miR-31-5p介导的PI3K/AKT/Bcl-2信号通路上调所必需的。

结论

我们的研究结果提供了关于miR-31-5p/ 通过PI3K/AKT/Bcl-2信号通路在22RV1细胞增殖和凋亡中的潜在机制的信息。这些结果表明,miR-31-5p和14-3-3ε可能潜在地用作PCa治疗的新型预后标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/0538d64e8f55/CMAR-12-6679-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/404173690aa9/CMAR-12-6679-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/4a8066f14c61/CMAR-12-6679-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/11f0291d9b18/CMAR-12-6679-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/b3a67d24ee57/CMAR-12-6679-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/81810f6d108e/CMAR-12-6679-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/3f20385a425f/CMAR-12-6679-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/6fa63c022d29/CMAR-12-6679-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/7cbc2b94dde8/CMAR-12-6679-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/0538d64e8f55/CMAR-12-6679-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/404173690aa9/CMAR-12-6679-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/4a8066f14c61/CMAR-12-6679-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/11f0291d9b18/CMAR-12-6679-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/b3a67d24ee57/CMAR-12-6679-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/81810f6d108e/CMAR-12-6679-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/3f20385a425f/CMAR-12-6679-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/6fa63c022d29/CMAR-12-6679-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/7cbc2b94dde8/CMAR-12-6679-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b029/7402864/0538d64e8f55/CMAR-12-6679-g0009.jpg

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