Epigenetics in metal carcinogenesis: nickel, arsenic, chromium and cadmium.
Although carcinogenic metals have been known to disrupt a wide range of cellular processes the precise mechanism by which these exert their carcinogenic effects is not known. Over the last decade or two, studies in the field of metal carcinogenesis suggest that epigenetic mechanisms may play a role in metal-induced carcinogenesis. In this review we summarize the evidence demonstrating that exposure to carcinogenic metals such as nickel, arsenic, chromium, and cadmium can perturb DNA methylation levels as well as global and gene specific histone tail posttranslational modification marks. We also wish to emphasize the importance in understanding that gene expression can be regulated by both genetic and epigenetic mechanisms and both these must be considered when studying the mechanism underlying the toxicity and cell-transforming ability of carcinogenic metals and other toxicants, and aberrant changes in gene expression that occur during disease states such as cancer.
Arita
Adriana
A
Nelson Institute of Environmental Medicine, New York University School of Medicine, NY 10987, USA.
Costa
Max
M
D000818:Animals; D001151:Arsenic / Q000633:toxicity; D020261:Arsenic Poisoning / Q000235:genetics; D002471:Cell Transformation, Neoplastic / Q000187:drug effects* / Q000235:genetics*; D019175:DNA Methylation; D057890:Epigenomics; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D000075322:Heavy Metal Poisoning; D006801:Humans; D019216:Metals, Heavy / Q000633:toxicity*
D019216:Metals, Heavy; D001151:Arsenic
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