ArticlePloS one2015
Arsenic Trioxide Reduces Global Histone H4 Acetylation at Lysine 16 through Direct Binding to Histone Acetyltransferase hMOF in Human Cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- Immune-epigenetic convergence in biomaterial-guided tissue regeneration.Materials today. Bio · 2026Article
- KAT8-mediated epigenetic modifications: Physiological functions, heterogeneity in disease, and advances in targeted development.iScience · 2026Review
- Integration of epigenetics into ecotoxicology: insights and fundamental research needs.Biological reviews of the Cambridge Philosophical Society · 2026Review
- Impact of Arsenite on Transient and Persistent Histone H3 Modifications and Transcriptional Response.Chemical research in toxicology · 2026Article
- Histone modification changes upon exposure of human lung adenocarcinoma cells to nanoparticles.Scientific reports · 2025Article
- Research progress on the regulatory mechanism of cell senescence in arsenic toxicity: a systematic review.Toxicology research · 2024Review
- hMOF induces cisplatin resistance of ovarian cancer by regulating the stability and expression of MDM2.Cell death discovery · 2023Article
- Negative Impacts of Arsenic on Plants and Mitigation Strategies.Plants (Basel, Switzerland) · 2023Review
- Epigenomic reprogramming in iAs-mediated carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- HDAC4 in cancer: A multitasking platform to drive not only epigenetic modifications.Frontiers in molecular biosciences · 2023Review
- Review
- The Roles of Histone Post-Translational Modifications in the Formation and Function of a Mitotic Chromosome.International journal of molecular sciences · 2022Review
- Natural Bioactive Compounds Targeting Histone Deacetylases in Human Cancers: Recent Updates.Molecules (Basel, Switzerland) · 2022Review
- Epigenetic Regulation in Exposome-Induced Tumorigenesis: Emerging Roles of ncRNAs.Biomolecules · 2022Review
- Recent progress in DNA methyltransferase inhibitors as anticancer agents.Frontiers in pharmacology · 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
- Anticancer mechanisms of phytochemical compounds: focusing on epigenetic targets.Environmental science and pollution research international · 2021Review
- KAT8/MOF-Mediated Anti-Cancer Mechanism of Gemcitabine in Human Bladder Cancer Cells.Biomolecules & therapeutics · 2021Article
- Epigenetic Effects of Nanomaterials and Nanoparticles.Journal of nanobiotechnology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone post-translational modification heritably regulates gene expression involved in most cellular biological processes. Experimental studies suggest that alteration of histone modifications affects gene expression by changing chromatin structure, causing various cellular responses to environmental influences. Arsenic (As), a naturally occurring element and environmental pollutant, is an established human carcinogen. Recently, increasing evidence suggests that As-mediated epigenetic mechanisms may be involved in its toxicity and carcinogenicity, but how this occurs is still unclear. Here we present evidence that suggests As-induced global histone H4K16 acetylation (H4K16ac) partly due to the direct physical interaction between As and histone acetyltransferase (HAT) hMOF (human male absent on first) protein, leading to the loss of hMOF HAT activity. Our data show that decreased global H4K16ac and increased deacetyltransferase HDAC4 expression occurred in arsenic trioxide (As2O3)-exposed HeLa or HEK293T cells. However, depletion of HDAC4 did not affect global H4K16ac, and it could not raise H4K16ac in cells exposed to As2O3, suggesting that HDAC4 might not directly be involved in histone H4K16 de-acetylation. Using As-immobilized agarose, we confirmed that As binds directly to hMOF, and that this interaction was competitively inhibited by free As2O3. Also, the direct interaction of As and C2CH zinc finger peptide was verified by MAIDI-TOF mass and UV absorption. In an in vitro HAT assay, As2O3 directly inhibited hMOF activity. hMOF over-expression not only increased resistance to As and caused less toxicity, but also effectively reversed reduced H4K16ac caused by As exposure. These data suggest a theoretical basis for elucidating the mechanism of As toxicity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.