ArticleToxicology and applied pharmacology2009
Modulation of histone methylation and MLH1 gene silencing by hexavalent chromium.
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 69 papers.
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Who cites it
69 citing papers in PubMed, 162 citations in OpenAlex.
- Environmental influences on macrophage epigenetics and trained immunity: a review.Molecular biology reports · 2026Review
- Sex differences in gastric cancer mutational burden reflect MLH1-associated epigenetic regulation.BMC cancer · 2026Article
- Epigenetic mechanisms linking hexavalent chromium exposure to pancreatic cancer risk: a systematic review.Environmental epigenetics · 2026Review
- Trivalent chromium interacts directly with acetylated lysine.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025Article
- Molecular signatures under hexavalent chromium, particulate matter 2.5, and cigarette smoking exposures.Discover oncology · 2025Article
- Environmental Xenobiotics and Epigenetic Modifications: Implications for Human Health and Disease.Journal of xenobiotics · 2025Review
- Particulate hexavalent chromium inhibits global transcription of genes in DNA repair pathways, particularly targeting homologous recombination repair, base excision repair, mismatch repair and microhomology-mediated end-joining.Journal of hazardous materials · 2025Article
- Heavy metals: toxicity and human health effects.Archives of toxicology · 2025Review
- Role of PERK-Mediated Endoplasmic Reticulum Stress in Ferroptosis Caused by Hexavalent Chromium in Chicken Hepatocytes.Biological trace element research · 2024Article
- Chromate Affects Gene Expression and DNA Methylation in Long-Term In Vitro Experiments in A549 Cells.International journal of molecular sciences · 2024Article
- How Does Environmental and Occupational Exposure Contribute to Carcinogenesis in Genitourinary and Lung Cancers?Cancers · 2023Review
- Hexavalent chromium-induced epigenetic instability and transposon activation lead to phenotypic variations and tumors inEnvironmental epigenetics · 2023Article
- Epigenetic and epitranscriptomic mechanisms of chromium carcinogenesis.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Review
- Impact of Nano- and Micro-Sized Chromium(III) Particles on Cytotoxicity and Gene Expression Profiles Related to Genomic Stability in Human Keratinocytes and Alveolar Epithelial Cells.Nanomaterials (Basel, Switzerland) · 2022Article
- Epigenetic mechanisms in metal carcinogenesis.Toxicology reports · 2022Review
- Current understanding of hexavalent chromium [Cr(VI)] neurotoxicity and new perspectives.Environment international · 2022Review
- Ascorbate: antioxidant and biochemical activities and their importance for in vitro models.Archives of toxicology · 2021Review
- Hexavalent chromium disrupts chromatin architecture.Seminars in cancer biology · 2021Review
- Lung Cancer Occurrence-Correlation with Serum Chromium Levels and Genotypes.Biological trace element research · 2021Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hexavalent chromium [Cr(VI)] is a mutagen and carcinogen, and occupational exposure can lead to lung cancers and other adverse health effects. Genetic changes resulting from DNA damage have been proposed as an important mechanism that mediates chromate's carcinogenicity. Here we show that chromate exposure of human lung A549 cells increased global levels of di- and tri-methylated histone H3 lysine 9 (H3K9) and lysine 4 (H3K4) but decreased the levels of tri-methylated histone H3 lysine 27 (H3K27) and di-methylated histone H3 arginine 2 (H3R2). Most interestingly, H3K9 dimethylation was enriched in the human MLH1 gene promoter following chromate exposure and this was correlated with decreased MLH1 mRNA expression. Chromate exposure increased the protein as well as mRNA levels of G9a a histone methyltransferase that specifically methylates H3K9. This Cr(VI)-induced increase in G9a may account for the global elevation of H3K9 dimethylation. Furthermore, supplementation with ascorbate, the primary reductant of Cr(VI) and also an essential cofactor for the histone demethylase activity, partially reversed the H3K9 dimethylation induced by chromate. Thus our studies suggest that Cr(VI) may target histone methyltransferases and demethylases, which in turn affect both global and gene promoter specific histone methylation, leading to the silencing of specific tumor suppressor genes such as MLH1.
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Registered trials
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.