MicroRNA-107 inhibits proliferation of prostate cancer cells by targeting cyclin E1
MicroRNA-107 inhibits proliferation of prostate cancer cells by targeting cyclin E1
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MicroRNA-107 通过靶向细胞周期蛋白 E1 抑制前列腺癌细胞增殖
DOI：
10.4149/neo_2018_181105n825
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发表时间：
2019-01-01
期刊：
影响因子：
3
通讯作者：
Xie, L. P.
中科院分区：
文献类型：
--
作者：
Zhang, X.;Jin, K.;Xie, L. P.
先前的研究报道，miR - 107可作为前列腺癌（PCa）潜在的外周生物标志物。然而，miR - 107在前列腺癌中的具体功能及其相关机制仍不清楚。本研究的目的是探究miR - 107在前列腺癌中的细胞功能并揭示相关机制。采用微小RNA加尾定量实时聚合酶链反应（qRT - PCR）来检测miR - 107在前列腺癌细胞系DU145和PC3以及正常前列腺细胞系RWPE - 1中的表达。通过显色原位杂交（CISH）确定miR - 107在前列腺癌组织和配对的癌旁组织中的表达模式。通过细胞活力、集落形成、流式细胞仪细胞周期和凋亡、划痕愈合以及Transwell迁移实验来研究miR - 107在前列腺癌细胞中的功能。此外，进行qRT - PCR、蛋白质印迹分析和双荧光素酶报告基因实验以验证miR - 107在前列腺癌中的靶标。结果表明，与正常前列腺细胞和癌旁组织相比，miR - 107在前列腺癌细胞和组织中表达下调，并且miR - 107的过表达抑制前列腺癌细胞的增殖并诱导G1/S期阻滞，但对前列腺癌细胞的凋亡或细胞运动没有影响。发现miR - 107通过直接结合细胞周期蛋白E1（CCNE1）的3' - 非翻译区而将其作为前列腺癌细胞中的靶标。总之，miR - 107可能是前列腺癌中一种潜在的肿瘤抑制因子，恢复miR - 107可能为前列腺癌提供一种新的治疗选择。
Previous studies have reported that miR-107 could be utilized as a potential peripheral biomarker in prostate cancer (PCa). However, the specific functions of miR-107 in prostate cancer and its relevant mechanisms are still unknown. The aim of this research was to investigate the cellular functions of miR-107 in PCa and reveal the relevant mechanisms. MicroRNA tailing quantitative real-time PCR (qRT-PCR) was adopted to measure the expression of miR-107 in PCa cell line DU145 and PC3, as well as in normal prostate cell line RWPE-1. The miR-107 expression pattern in PCa tissues and paired peritumoral tissues were determined by Chromogenic In Situ Hybridization (CISH). Cell viability, colony formation, flow cytometry cell cycle and apoptosis, wound healing and Transwell migration assays were performed to study the miR-107 functions in PCa cells. Further, qRT-PCR, western blot analysis and dual-luciferase reporter assays were conducted to verify the target of miR-107 in PCa. Results demonstrated that miR-107 was downregulated in PCa cells and tissues in comparison with normal prostate cells and peritumoral tissues, and the over-expression of miR-107 suppressed proliferation and induced G1/S arrest of PCa cells but had no effects on apoptosis or cell motility of PCa cells. MiR-107 was found to target cyclin E1 (CCNE1) in PCa cells by directly binding to its 3'-UTR. In conclusion, miR-107 could be a potential tumor suppressor in PCa, and the restoration of miR-107 might provide a new therapeutic option for PCa.