MicroRNA‐505‐3p mediates cell motility of epithelial ovarian cancer via suppressing PEAK1 expression

Author:

Wu Yanni1,Xue Lei1,Xiong Wei2,Li Haiyang2,Wu Jiao1,Xie Wei1,Long Ying1ORCID,Liu Ying1,Luo Chenhui1

Affiliation:

1. Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine Central South University Changsha Hunan China

2. Hunan Traditional Chinese Medical College Zhuzhou Hunan China

Abstract

AbstractMicroRNAs (miRNAs) are a class of small RNA genes with important roles in cancer biology regulation. There are considerable studies regarding the roles of microRNA‐505‐3p (miR‐505‐3p) in cancer development and progression, but the function of miR‐505‐3p in epithelial ovarian cancer (EOC) has not been fully clarified. Comparative analysis of miRNA expression data set was used to select differentially expressed miRNAs. Quantitative real‐time polymerase chain reaction was applied to detect expression levels of RNAs, while western blot and immunofluorescence staining were performed to detect expression levels of proteins of interest. The motility of EOC cells was assessed by wound healing and transwell assays. The binding and regulating relationship between miRNA and its direct target gene was investigated by dual‐luciferase assay. Our results show that miR‐505‐3p was upregulated in recurrent EOC, which significantly inhibits EOC cell motility via modulating cell epithelial–mesenchymal transition. Furthermore, our results indicated that PEAK1 expression was inhibited by direct binding of miR‐505‐3p into its 3′‐URT in EOC cells. Importantly, knockdown of PEAK1 attenuated the effect of mi‐505‐3p inhibitor on EOC cell migration and invasion. In conclusion, our findings indicate that miRNA‐505‐3p inhibits EOC cell motility by targeting PEAK1.

Publisher

Wiley

Cited by 1 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3