期刊
CELLULAR SIGNALLING
卷 26, 期 6, 页码 1335-1346出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2014.03.001
关键词
Myocardin; Maspin; Epigenetic modification; Apoptosis
类别
资金
- National Natural Science Foundation of China [30970615, 31071126, 31000343, 31171303, 31171297, 31200955]
- Program for Changjiang Scholars and Innovative Research Team in University of Ministry of Education of the People's Republic of China [IRT1166]
- Research Fund for the Doctoral Program of Higher Education of China [20111208110001]
- Key Project of Chinese Ministry of Education [212010]
Breast cancer is the leading cause of cancer death in women worldwide. It is well known that oncogene activation and anti-oncogene inactivation affect the development and progression of breast cancer, but the role of oncogene activation and anti-oncogene inactivation in breast cancer is still not fully understood. We now report that maspin acts as a tumor suppressor gene to induce MCF-7 cell apoptosis. In addition, maspin promoter hypermethylation and histone hypoacetylation lead to silencing of maspin gene expression in MCF-7 cells. Moreover, DNA methyltransferase (DNMT) inhibitor 5-aza-2 '-deoxycytidine (5-aza-dc) and/or the histone deacetylase (HDAC) inhibitor Trichostatin A (TSA) strongly up-regulated the expression of maspin in MCF-7 cells. Notably, myocardin can promote the re-expression of maspin in MCF-7 cells. Luciferase assay shows that myocardin activates the transcription of maspin promoter by CArG box. More importantly, 5-aza-dc/FSA and myocardin synergetically enhance re-expression of maspin and augment maspin-mediated apoptosis in MCF-7 cells. Thus, these data reveal the new insight that myocardin meditates apoptosis in breast cancer through affecting maspin reexpression and epigenetic modification to regulate the development of breast cancer, thereby raising the possibility of its use in breast cancer therapy. (C) 2014 Elsevier B.V. All rights reserved.
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