Abstract Arsenic is a toxic metalloid widely present in the earth’s crust, and is a proven human carcinogen. Chronic arsenic exposure mainly through drinking water causes skin, lung and urinary bladder cancers, and is associated with liver, prostate and kidney cancers, cardiovascular and neurological disorders, and diabetes. Several modes of action have been suggested in arsenic carcinogenesis. However, the molecular etiology of arsenic induced cancer remains unclear. Recent evidence clearly indicates that gene expression modifications induced by arsenic may involve epigenetic alterations, including miRNA dysregulation. Many miRNAs have been implicated in different human cancers as a consequence of losses and or gains of miRNA function that contribute to cancer development. Progress in identifying miRNA dysregulation induced by arsenic has been made using different approaches and models. The present review discusses the recent data regarding dysregulated expression of miRNA in arsenic-induced malignant transformation in vitro, gaps in current understanding and deficiencies in current models for arsenic-induced carcinogenesis, and future directions of research that would improve our knowledge regarding the mechanisms involved in arsenic-induced carcinogenesis. © The Author(s) 2018. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: email@example.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)
Toxicological Sciences – Oxford University Press
Published: May 28, 2018
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