miR-22-3p/PGC1β Suppresses Breast Cancer Cell Tumorigenesis via PPARγ.

IF 3.5 3区医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL

PPAR Research Pub Date : 2021-03-12 eCollection Date: 2021-01-01 DOI:10.1155/2021/6661828

Xuehui Wang, Zhilu Yao, Lin Fang

引用次数: 16

Abstract

In this study, we found that miR-22-3p expression was decreased in breast cancer (BC) cell lines and tissues. Overexpression of miR-22-3p inhibited the proliferation and migration of BC cells in vitro and in vivo, while depletion of miR-22-3p exhibited the opposite effect. Importantly, miR-22-3p could directly target PGC1β and finally regulate the PPARγ pathway in BC. In conclusion, miR-22-3p/PGC1β suppresses BC cell tumorigenesis via PPARγ, which may become a potential biomarker and therapeutic target.

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miR-22-3p/PGC1β通过PPARγ抑制乳腺癌细胞的肿瘤发生

在本研究中，我们发现miR-22-3p在乳腺癌细胞系和组织中表达降低。在体外和体内，过表达miR-22-3p抑制了BC细胞的增殖和迁移，而缺失miR-22-3p则表现出相反的效果。重要的是，miR-22-3p可以直接靶向PGC1β并最终调节BC中的PPARγ通路。总之，miR-22-3p/PGC1β通过PPARγ抑制BC细胞的肿瘤发生，可能成为潜在的生物标志物和治疗靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

PPAR Research MEDICINE, RESEARCH & EXPERIMENTAL-

CiteScore

6.20

自引率

3.40%

发文量

审稿时长

12 months

期刊介绍： PPAR Research is a peer-reviewed, Open Access journal that publishes original research and review articles on advances in basic research focusing on mechanisms involved in the activation of peroxisome proliferator-activated receptors (PPARs), as well as their role in the regulation of cellular differentiation, development, energy homeostasis and metabolic function. The journal also welcomes preclinical and clinical trials of drugs that can modulate PPAR activity, with a view to treating chronic diseases and disorders such as dyslipidemia, diabetes, adipocyte differentiation, inflammation, cancer, lung diseases, neurodegenerative disorders, and obesity.