MiR-142-3p enhances chemosensitivity of breast cancer cells and inhibits autophagy by targeting HMGB1.
10.1016/j.apsb.2019.11.009
- Author:
Lu LIANG
1
;
Jijun FU
1
;
Siran WANG
2
;
Huiyu CEN
1
;
Lingmin ZHANG
1
;
Safur Rehman MANDUKHAIL
1
;
Lingran DU
1
;
Qianni WU
1
;
Peiquan ZHANG
1
;
Xiyong YU
1
Author Information
1. Key Laboratory of Molecular Target & Clinical Pharmacology and the State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences & the Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou 511436, China.
2. Department of Prosthodontics, the Second Affiliated Hospital of Harbin Medical University, Harbin 150001, China.
- Publication Type:Journal Article
- Keywords:
Breast cancer;
Chemosensitivity;
Drug resistance;
HMGB1;
MCF-7 cell line;
MiR-142-3p
- From:
Acta Pharmaceutica Sinica B
2020;10(6):1036-1046
- CountryChina
- Language:English
-
Abstract:
MiR-142-3p has been reported to act as a tumor suppressor in breast cancer. However, the regulatory effect of miR-142-3p on drug resistance of breast cancer cells and its underlying mechanism remain unknown. Here, we found that miR-142-3p was significantly downregulated in the doxorubicin (DOX)-resistant MCF-7 cell line (MCF-7/DOX). MiR-142-3p overexpression increased DOX sensitivity and enhanced DOX-induced apoptosis in breast cancer cells. High-mobility group box 1 (HMGB1) is a direct functional target of miR-142-3p in breast cancer cells and miR-142-3p negatively regulated HMGB1 expression. Moreover, overexpression of HMGB1 dramatically reversed the promotion of apoptosis and inhibition of autophagy mediated by miR-142-3p up-regulation. In conclusion, miR-142-3p overexpression may inhibit autophagy and promote the drug sensitivity of breast cancer cells to DOX by targeting HMGB1. The miR-142-3p/HMGB1 axis might be a novel target to regulate the drug resistance of breast cancer patients.
