MiR-142-3p enhances chemosensitivity of breast cancer cells and inhibits autophagy by targeting HMGB1

被引:1
|
作者
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 ]
机构
[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
[2] Department of Prosthodontics,the Second Affiliated Hospital of Harbin Medical University
基金
中国国家自然科学基金;
关键词
D O I
暂无
中图分类号
R737.9 [乳腺肿瘤];
学科分类号
摘要
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 DOXinduced 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,overexpres sion 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 HMGB 1.The miR-142-3 p/HMGB1 axis might be a novel target to regulate the drug resistance of breast cancer patients.
引用
收藏
页码:1036 / 1046
页数:11
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