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Updated: Feb 8, 2026
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Chromatin Immunoprecipitation ChIP to Assay Dynamic Histone Modification in Activated Gene Expression in Human Cells
Published on: July 29, 2010
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Mapping dynamic histone modification patterns during arsenic-induced malignant transformation of human bladder cells
Yichen Ge1, Jinqiu Zhu1, Xue Wang2
1Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, The State University of New York, Buffalo, NY 14214, USA.
Toxicology and Applied Pharmacology
|July 4, 2018
Summary
Arsenic exposure alters histone modifications, specifically increasing H3 acetylation and decreasing H4 acetylation, contributing to bladder cancer development. These epigenetic changes in histone acetylation and methylation are key to understanding arsenic carcinogenesis.
Area of Science:
- Environmental Toxicology
- Epigenetics
- Cancer Research
Background:
- Arsenic is a known risk factor for bladder cancer.
- Epigenetic alterations, including DNA methylation and histone posttranslational modifications (PTMs), are implicated in arsenic-induced carcinogenesis.
- Previous studies linked monomethylarsonous acid (MMAIII) exposure to altered histone acetylation in urothelial cells, correlating with malignant transformation.
Purpose of the Study:
- To identify and quantify diverse PTM patterns during MMAIII-induced malignant transformation using LC-MS/MS.
- To investigate the dynamic changes in histone acetylation and methylation induced by MMAIII exposure.
Main Methods:
- Utilized high-resolution, high-throughput liquid chromatography tandem mass spectrometry (LC-MS/MS).
- Analyzed histone PTMs in MMAIII-exposed human urothelial cells (UROtsa).
- Compared histone PTMs in leukocytes from individuals with high versus low arsenic exposure.
Main Results:
- MMAIII exposure induced time-dependent increases in histone H3 acetylation (K4, K9, K14, K18, K23, K27) and decreases in histone H4 acetylation (K5, K8, K12, K16).
- Observed increased H3K18ac and decreased H4K8ac in leukocytes of high arsenic-exposed individuals.
- MMAIII altered histone methylation, causing loss of H3K4me1 and increases in H3K9me1 and H3K27me1.
Conclusions:
- Arsenic exposure induces dynamic changes in histone acetylation and methylation patterns during cancer development.
- These epigenetic modifications are crucial in the mechanism of arsenic-induced carcinogenesis.
- Further research into the genomic locations of altered histone marks and resultant gene expression is essential.
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