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

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 cou...

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Main Authors: Xuehui Wang, Zhilu Yao, Lin Fang
Format: Article
Language:English
Published: Wiley 2021-01-01
Series:PPAR Research
Online Access:http://dx.doi.org/10.1155/2021/6661828
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author Xuehui Wang
Zhilu Yao
Lin Fang
author_facet Xuehui Wang
Zhilu Yao
Lin Fang
author_sort Xuehui Wang
collection DOAJ
description 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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institution Kabale University
issn 1687-4757
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language English
publishDate 2021-01-01
publisher Wiley
record_format Article
series PPAR Research
spelling doaj-art-4c89f2ca3ede44f99cdf31f638ddab1f2025-02-03T06:43:49ZengWileyPPAR Research1687-47571687-47652021-01-01202110.1155/2021/66618286661828miR-22-3p/PGC1β Suppresses Breast Cancer Cell Tumorigenesis via PPARγXuehui Wang0Zhilu Yao1Lin Fang2Department of Thyroid and Breast Surgery, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai 200072, ChinaDepartment of Thyroid and Breast Surgery, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai 200072, ChinaDepartment of Thyroid and Breast Surgery, Shanghai Tenth People’s Hospital, School of Medicine, Tongji University, Shanghai 200072, ChinaIn 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.http://dx.doi.org/10.1155/2021/6661828
spellingShingle Xuehui Wang
Zhilu Yao
Lin Fang
miR-22-3p/PGC1β Suppresses Breast Cancer Cell Tumorigenesis via PPARγ
PPAR Research
title miR-22-3p/PGC1β Suppresses Breast Cancer Cell Tumorigenesis via PPARγ
title_full miR-22-3p/PGC1β Suppresses Breast Cancer Cell Tumorigenesis via PPARγ
title_fullStr miR-22-3p/PGC1β Suppresses Breast Cancer Cell Tumorigenesis via PPARγ
title_full_unstemmed miR-22-3p/PGC1β Suppresses Breast Cancer Cell Tumorigenesis via PPARγ
title_short miR-22-3p/PGC1β Suppresses Breast Cancer Cell Tumorigenesis via PPARγ
title_sort mir 22 3p pgc1β suppresses breast cancer cell tumorigenesis via pparγ
url http://dx.doi.org/10.1155/2021/6661828
work_keys_str_mv AT xuehuiwang mir223ppgc1bsuppressesbreastcancercelltumorigenesisviapparg
AT zhiluyao mir223ppgc1bsuppressesbreastcancercelltumorigenesisviapparg
AT linfang mir223ppgc1bsuppressesbreastcancercelltumorigenesisviapparg