MiR‐600 mediates EZH2/RUNX3 signal axis to modulate breast cancer cell viability and sorafenib sensitivity

Author:

Zhao Qian1,Li Dan1,Feng Jinchun1,Jinsihan Dilixiati1ORCID

Affiliation:

1. Department of Breast Surgery The Affiliated Tumor Hospital of Xinjiang Urumqi China

Abstract

AbstractBreast cancer (BC) ranks as the most prevalent gynecologic tumor globally. Abnormal expression of miRNAs is concerned with the development of cancers such as BC. However, little is known about the role of miR‐600 in BC. This work aimed to explore the role of miR‐600 in the malignant progression and sorafenib sensitivity of BC cells. Expression and interaction of miR‐600/EZH2/RUNX3 were analyzed by bioinformatics. qRT‐PCR was utilized to assay RNA expression of miR‐600 and mRNA expression of EZH2/RUNX3. The binding relationship between miR‐600 and EZH2 was tested by dual luciferase assay and RNA immunoprecipitation (RIP). The effects of miR‐600/EZH2/RUNX3 axis on the malignant behavior and sorafenib sensitivity of BC cells were detected by CCK‐8 and colony formation assay. Low expression of miR‐600 and RUNX3 in BC was found by bioinformatics and molecular assays. High expression of EZH2 in BC was negatively correlated with RUVX3. Dual luciferase assay and RIP demonstrated that MiR‐600 could bind to EZH2. Cell assays displayed that miR‐600 knockdown could foster the malignant progression of BC cells and reduce the sensitivity of BC cells to sorafenib. EZH2 knockdown or RUNX3 overexpression could offset the effect of miR‐600 inhibitor on the malignant behavior and sorafenib sensitivity of BC cells. MiR‐600 can hinder the malignant behavior of BC cells and foster sensitivity of BC cells to sorafenib via EZH2/RUNX3 axis, exhibiting the miR‐600/EZH2/RUNX3 axis as a feasible therapeutic target for BC patients.

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Toxicology,Molecular Biology,Molecular Medicine,Biochemistry,General Medicine

Cited by 2 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