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Evidence of histone modification affecting ARID1A expression in colorectal cancer cell lines
Mehran Erfani1,2, Mozhdeh Zamani3, Pooneh Mokarram1,3
1Department of Biochemistry, Faculty of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Aim:
The current study aimed to focus on the role of histone deacetylation in reduced ARID1A expression in colorectal cancer cell lines.
Background:
ARID1A, a subunit of the switch/sucrose nonfermentable chromatin remodeling complex, has emerged as a bona fide tumor suppressor and is frequently downregulated and inactivated in multiple human cancers. Epigenetic modifications play an important role in dysregulation of gene expression in cancer. DNA methylation has been reported as an important regulator of ARID1A expression in colorectal cancer cell lines; however, the histone modification role in ARID1A suppression in colorectal cancer remains unclear.
Methods:
The expression levels of ARID1A mRNA were determined using real-time quantitative PCR in colorectal cancer cell lines including HCT116, SW48, HT29, SW742, LS180, and SW480. To evaluate the effect of histone deacetylation on ARID1A expression, all cell lines were treated with trichostatin A (TSA), a histone deacetylase inhibitor. SPSS software (Version 23) and GraphPad Prism (Version 6.01) were applied for data analysis using one-way ANOVA, followed by Tukey's multiple comparison tests.
Results:
Treatment of colorectal cancer cell lines with TSA increased ARID1A expression in a cell line-dependent manner, suggesting that histone deacetylation is at least one factor contributing to ARID1A downregulation in colorectal cancer.
Conclusion:
Histone deacetylase inhibitors might provide a strategy to restore ARID1A expression and may bring benefits to the colorectal cancer patients with a broader range of genetic backgrounds.
Insights
Histone deacetylation reduces ARID1A expression in colorectal cancer. Inhibiting histone deacetylases with TSA increased ARID1A levels, suggesting a therapeutic strategy for colorectal cancer patients.
Area of Science:
- Molecular oncology
- Epigenetics
- Cancer biology
Background:
- ARID1A, a tumor suppressor, is frequently inactivated in cancers.
- Epigenetic modifications, including DNA methylation, impact ARID1A expression.
- The role of histone modifications in ARID1A suppression in colorectal cancer was unclear.
Purpose of the Study:
- To investigate the role of histone deacetylation in ARID1A downregulation.
- To assess the effect of histone deacetylase inhibitors on ARID1A expression in colorectal cancer cell lines.
Main Methods:
- ARID1A mRNA levels were quantified using real-time quantitative PCR.
- Colorectal cancer cell lines were treated with trichostatin A (TSA), a histone deacetylase inhibitor.
- Statistical analysis was performed using ANOVA and Tukey's multiple comparison tests.
Main Results:
- TSA treatment increased ARID1A expression in a cell line-dependent manner.
- This suggests histone deacetylation contributes to ARID1A downregulation in colorectal cancer.
- ARID1A expression varied across different colorectal cancer cell lines.
Conclusions:
- Histone deacetylation is implicated in reduced ARID1A expression in colorectal cancer.
- Histone deacetylase inhibitors may offer a therapeutic approach to restore ARID1A levels.
- Targeting histone deacetylation could benefit a wider range of colorectal cancer patients.
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