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微小RNA-154-5p通过靶向E2F5抑制前列腺癌细胞系的增殖、迁移和侵袭。

miRNA-154-5p Inhibits Proliferation, Migration and Invasion by Targeting E2F5 in Prostate Cancer Cell Lines.

作者信息

Zheng Yang, Zhu Chen, Ma Long, Shao Pengfei, Qin Chao, Li Pu, Cao Qiang, Ju Xiaobing, Cheng Gong, Zhu Qingyi, Gu Xiaojian, Hua Lixin

机构信息

Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

出版信息

Urol Int. 2017;98(1):102-110. doi: 10.1159/000445252. Epub 2016 Apr 14.

Abstract

BACKGROUND

MicroRNAs (miRNAs) are a class of small non-coding RNAs (18-25 nucleotides) which post-transcriptionally regulate gene expression by negatively regulating the stability or translational efficiency of their target mRNAs. This study aimed to determine the function of miR-154-5p in prostate cancer (PCa) cells and identify the novel molecular targets regulated by miR-154-5p.

MATERIALS AND METHODS

The effects of forced miR-154-5p expression or E2F transcription factor 5 (E2F5) knockdown on PCa cells were evaluated by cell proliferation, flow cytometry, cell migration and invasion assays as well as by Western blot analysis. Dual-luciferase reporter assay was performed to verify the precise target of miR-154-5p.

RESULTS

The forced expression of miR-154-5p or E2F5 knockdown significantly restrained cell growth, as well as the migratory and invasive capabilities. Such expression also induced G1 cell cycle arrest of PCa cells in vitro. Hence, E2F5 is a direct target gene of miR-154-5p.

CONCLUSIONS

miR-154-5p may play an important role as an inhibitor of proliferation, migration and invasion of PCa by targeting E2F5 in PCa cell lines.

摘要

背景

微小RNA(miRNA)是一类小的非编码RNA(18 - 25个核苷酸),通过负向调节其靶mRNA的稳定性或翻译效率在转录后调节基因表达。本研究旨在确定miR - 154 - 5p在前列腺癌(PCa)细胞中的功能,并鉴定受miR - 154 - 5p调节的新分子靶点。

材料与方法

通过细胞增殖、流式细胞术、细胞迁移和侵袭试验以及蛋白质免疫印迹分析,评估强制表达miR - 154 - 5p或敲低E2F转录因子5(E2F5)对PCa细胞的影响。进行双荧光素酶报告基因检测以验证miR - 154 - 5p的精确靶点。

结果

强制表达miR - 154 - 5p或敲低E2F5显著抑制细胞生长以及迁移和侵袭能力。这种表达还在体外诱导PCa细胞的G1期细胞周期阻滞。因此,E2F5是miR - 154 - 5p的直接靶基因。

结论

在PCa细胞系中,miR - 154 - 5p可能通过靶向E2F5作为PCa增殖、迁移和侵袭的抑制剂发挥重要作用。

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