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Updated: May 2, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Re-expression and epigenetic modification of maspin induced apoptosis in MCF-7 cells mediated by myocardin
Xing-Hua Liao1, Yan-Qi Li2, Nan Wang2
1Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education and Tianjin, College of Biotechnology, Tianjin University of Science and Technology, 300457, PR China; Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China.
Abstract:
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/TSA 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 re-expression and epigenetic modification to regulate the development of breast cancer, thereby raising the possibility of its use in breast cancer therapy.
Insights
Maspin acts as a tumor suppressor gene in breast cancer. Myocardin can re-express maspin, inducing apoptosis and offering potential new breast cancer therapies.
Area of Science:
- Molecular Biology
- Cancer Research
- Epigenetics
Background:
- Breast cancer is a leading cause of cancer death in women globally.
- Understanding oncogene and anti-oncogene roles is crucial for breast cancer progression.
- The tumor suppressor function of maspin in breast cancer requires further elucidation.
Purpose of the Study:
- To investigate the role of maspin as a tumor suppressor in breast cancer.
- To explore the epigenetic regulation of maspin gene expression.
- To examine the effect of myocardin on maspin re-expression and breast cancer cell apoptosis.
Main Methods:
- MCF-7 breast cancer cells were used to study maspin expression and apoptosis.
- Epigenetic modifications (hypermethylation, hypoacetylation) were investigated.
- Inhibitors of DNA methyltransferase (5-aza-dc) and histone deacetylase (TSA) were applied.
- Myocardin's effect on maspin promoter transcription was analyzed using luciferase assays.
Main Results:
- Maspin functions as a tumor suppressor, inducing apoptosis in MCF-7 cells.
- Maspin gene expression is silenced by promoter hypermethylation and histone hypoacetylation.
- 5-aza-dc and TSA treatment significantly up-regulated maspin expression.
- Myocardin activates maspin promoter transcription via the CArG box.
- Combined 5-aza-dc/TSA and myocardin treatment synergistically enhanced maspin re-expression and apoptosis.
Conclusions:
- Maspin acts as a tumor suppressor gene, inducing apoptosis in breast cancer cells.
- Epigenetic silencing of maspin can be reversed by DNMT and HDAC inhibitors.
- Myocardin promotes maspin re-expression and enhances maspin-mediated apoptosis.
- Myocardin's role in epigenetic regulation of maspin offers potential therapeutic strategies for breast cancer.
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