1. Oncogenomic disruptions in arsenic-induced carcinogenesis.
- Author
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Sage AP, Minatel BC, Ng KW, Stewart GL, Dummer TJB, Lam WL, and Martinez VD
- Subjects
- Animals, Chromosome Aberrations chemically induced, Epigenesis, Genetic drug effects, Gene Expression Regulation drug effects, Genetic Predisposition to Disease, Genetic Variation drug effects, Genomic Instability drug effects, Humans, Neoplasms pathology, RNA Interference, RNA, Untranslated genetics, Arsenic adverse effects, Carcinogenesis chemically induced, Neoplasms etiology, Neoplasms metabolism
- Abstract
Chronic exposure to arsenic affects more than 200 million people worldwide, and has been associated with many adverse health effects, including cancer in several organs. There is accumulating evidence that arsenic biotransformation, a step in the elimination of arsenic from the human body, can induce changes at a genetic and epigenetic level, leading to carcinogenesis. At the genetic level, arsenic interferes with key cellular processes such as DNA damage-repair and chromosomal structure, leading to genomic instability. At the epigenetic level, arsenic places a high demand on the cellular methyl pool, leading to global hypomethylation and hypermethylation of specific gene promoters. These arsenic-associated DNA alterations result in the deregulation of both oncogenic and tumour-suppressive genes. Furthermore, recent reports have implicated aberrant expression of non-coding RNAs and the consequential disruption of signaling pathways in the context of arsenic-induced carcinogenesis. This article provides an overview of the oncogenomic anomalies associated with arsenic exposure and conveys the importance of non-coding RNAs in the arsenic-induced carcinogenic process.
- Published
- 2017
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