Journal
EPIGENOMICS
Volume 2, Issue 1, Pages 87-104Publisher
FUTURE MEDICINE LTD
DOI: 10.2217/EPI.09.45
Keywords
arsenate; arsenic; arsenite; cancer; carcinogenesis; DNMT; epigenetics; glutathione; hypermethylation; hypomethylation; oxidative stress; S-adenosylmethionine; SAM; transsulfuration
Categories
Funding
- NIEHS [R01 ES06273, R01 ES10807]
- NIEHS Center for Environmental Genetics [P30 ES06096]
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Arsenic is a nonmutagenic human carcinogen that induces tumors through unknown mechanisms. A growing body of evidence suggests that its carcinogenicity results from epigenetic changes, particularly in DNA methylation. Changes in gene methylation status, mediated by arsenic, have been proposed to activate oncogene expression or silence tumor suppressor genes, leading to long-term changes in the activity of genes controlling cell transformation. Mostly descriptive, and often contradictory, studies have demonstrated that arsenic exposure is associated with both hypo- and hyper-methylation at various genetic loci in vivo or in vitro. This ambiguity has made it difficult to assess whether the changes induced by arsenic are causally involved in the transformation process or are simply a reflection of the altered physiology of rapidly dividing cancer cells. Here, we discuss the evidence supporting changes in DNA methylation as a cause of arsenic carcinogenesis and highlight the strengths and limitations of these studies, as well as areas where consistencies and inconsistencies exist.
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