ArticleToxicology and applied pharmacology2009
Acetylated H4K16 by MYST1 protects UROtsa cells from arsenic toxicity and is decreased following chronic arsenic exposure.
Article in Toxicology and applied pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 99 citations in OpenAlex.
- KAT8-mediated epigenetic modifications: Physiological functions, heterogeneity in disease, and advances in targeted development.iScience · 2026Review
- Nicotine-induced mitophagy in bronchial epithelial cells and MYST1 downregulation in cigarette smoke-exposed lungs: potential mechanisms of COPD progression.Molecular biology reports · 2026Article
- Research progress on the regulatory mechanism of cell senescence in arsenic toxicity: a systematic review.Toxicology research · 2024Review
- Arsenic and cancer: Evidence and mechanisms.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Epigenomic reprogramming in iAs-mediated carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Review
- Arsenic and Human Health: Genotoxicity, Epigenomic Effects, and Cancer Signaling.Biological trace element research · 2022Review
- Epigenetic mechanisms in metal carcinogenesis.Toxicology reports · 2022Review
- Arsenic-induced epigenetic changes in cancer development.Seminars in cancer biology · 2021Review
- Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications.International journal of molecular sciences · 2021Review
- Epigenetic influence of environmentally neurotoxic metals.Neurotoxicology · 2020Review
- Molecular Mechanisms of Arsenic-Induced Disruption of DNA Repair.Chemical research in toxicology · 2020Review
- The Promises and Challenges of Toxico-Epigenomics: Environmental Chemicals and Their Impacts on the Epigenome.Environmental health perspectives · 2020Article
- Sodium arsenite exposure inhibits histone acetyltransferase p300 for attenuating H3K27ac at enhancers in mouse embryonic fibroblast cells.Toxicology and applied pharmacology · 2018Article
- Mapping dynamic histone modification patterns during arsenic-induced malignant transformation of human bladder cells.Toxicology and applied pharmacology · 2018Article
- Chemical and genetic control of IFNγ-induced MHCII expression.EMBO reports · 2018Article
- Tricho-rhino-phalangeal syndrome 1 protein functions as a scaffold required for ubiquitin-specific protease 4-directed histone deacetylase 2 de-ubiquitination and tumor growth.Breast cancer research : BCR · 2018Article
- Effects of arsenic toxicity beyond epigenetic modifications.Environmental geochemistry and health · 2018Review
- Editor's Highlight: High-Throughput Functional Genomics Identifies Modulators of TCE Metabolite Genotoxicity and Candidate Susceptibility Genes.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Arsenite Binds to the Zinc Finger Motif of TIP60 Histone Acetyltransferase and Induces Its Degradation via the 26S Proteasome.Chemical research in toxicology · 2017Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Arsenic, a human carcinogen that is associated with an increased risk of bladder cancer, is commonly found in drinking water. An important mechanism by which arsenic is thought to be carcinogenic is through the induction of epigenetic changes that lead to aberrant gene expression. Previously, we reported that the SAS2 gene is required for optimal growth of yeast in the presence of arsenite (As(III)). Yeast Sas2p is orthologous to human MYST1, a histone 4 lysine 16 (H4K16) acetyltransferase. Here, we show that H4K16 acetylation is necessary for the resistance of yeast to As(III) through the modulation of chromatin state. We further explored the role of MYST1 and H4K16 acetylation in arsenic toxicity and carcinogenesis in human bladder epithelial cells. The expression of MYST1 was knocked down in UROtsa cells, a model of bladder epithelium that has been used to study arsenic-induced carcinogenesis. Silencing of MYST1 reduced acetylation of H4K16 and induced sensitivity to As(III) and to its more toxic metabolite monomethylarsonous acid (MMA(III)) at doses relevant to high environmental human exposures. In addition, both As(III) and MMA(III) treatments decreased global H4K16 acetylation levels in a dose- and time-dependent manner. This indicates that acetylated H4K16 is required for resistance to arsenic and that a reduction in its levels as a consequence of arsenic exposure may contribute to toxicity in UROtsa cells. Based on these findings, we propose a novel role for the MYST1 gene in human sensitivity to arsenic.
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