Stat5 inhibits NLRP3‐mediated pyroptosis to enhance chemoresistance of breast cancer cells via promoting miR‐182 transcription

Author:

Wan Peng1,He Xiaolan1,Han Ying1,Wang Liangliang1,Yuan Zuguo1

Affiliation:

1. Affiliated People's Hospital of Ningbo University Cancer Chemoradiotherapy Center Ningbo China

Abstract

AbstractThe treatment of breast cancer (BC) calls for targeted methods to overcome chemoresistance (CR). This study is expected to figure out the mechanism of signal transducer and activator of transcription 5 (STAT5) in NOD‐like receptor family pyrin domain containing 3 (NLRP3)‐mediated pyroptosis and CR in BC cells. BC cell lines resistant to paclitaxel (PTX) and cis‐diamminedichloro‐platinum (DDP) were prepared. Expressions of Stat5, miR‐182, and NLRP3 were detected. The 50% inhibition concentration (IC50), proliferation, colony formation, apoptosis rate, and levels of pyroptosis‐related factors were appraised and determined. The binding relationships of Stat5 and miR‐182, and miR‐182 and NLRP3 were testified. Stat5 and miR‐182 were highly expressed in drug‐resistant BC cells. Silencing Stat5 reduced proliferation and colony formation of drug‐resistant BC cells, coincided with elevated levels of pyroptosis‐related factors. Stat5 bound to the promoter region of miR‐182 to promote miR‐182 expression. miR‐182 inhibition reversed the role of silencing Stat5 in BC cells. miR‐182 inhibited NLRP3. Overall, Stat5 bound to the promoter region of miR‐182 to promote miR‐182 expression and inhibit NLRP3 transcription, thereby suppressing pyroptosis and enhancing CR of BC cells.

Publisher

Wiley

Subject

Molecular Medicine,Biochemistry,Drug Discovery,Pharmacology,Organic Chemistry

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