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Updated: Dec 22, 2025
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Obtaining Cancer Stem Cell Spheres from Gynecological and Breast Cancer Tumors
Published on: March 1, 2020
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Effect of epigenetic modulation on cancer sphere
Shuichi Iwahashi1, Mitsuo Shimada1, Yuji Morine1
1Department of Surgery, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.
The Journal of Medical Investigation : JMI
|May 8, 2020
Summary
Histone deacetylase (HDAC) inhibitors like valproic acid can reverse cancer stem cell properties by altering epigenetic modifications. This suggests a potential strategy to overcome treatment-resistant cancers through histone acetylation.
Area of Science:
- Oncology
- Epigenetics
- Molecular Biology
Background:
- Cancer stem cells drive treatment-resistant cancers.
- Epigenetic modifications, including DNA methylation and chromatin remodeling, are crucial in cancer development.
- Targeting epigenetic mechanisms offers a potential strategy against resistant tumors.
Purpose of the Study:
- To investigate the role of epigenetic modification in cancer stem cells.
- To explore the effects of a histone deacetylase (HDAC) inhibitor on cancer stem cell properties and epigenetic status.
Main Methods:
- Generated cancer spheres from HepG2 cells to model cancer stem cells.
- Treated cancer spheres with valproic acid (VPA), a HDAC inhibitor.
- Compared DNA methylation status and gene expression (using RT-PCR) between normal cells, cancer spheres, and VPA-treated spheres.
Main Results:
- Valproic acid (VPA) inhibited cancer sphere formation.
- Significant changes in DNA methylation were observed between normal HepG2 cells and cancer spheres, with identification of epithelial-mesenchymal transition (EMT) related genes.
- VPA treatment reduced the expression of EMT-related genes and Bcl-6 in cancer spheres.
- VPA also induced changes in DNA methylation status in cancer spheres.
Conclusions:
- HDAC inhibition impacts the DNA methylation landscape of cancer stem cells.
- Histone acetylation, modulated by HDAC inhibitors, may offer a therapeutic approach to overcome treatment resistance by regulating cancer stem cell populations.
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