Epigenetic Dysregulations in Arsenic-Induced Carcinogenesis

Simple Summary Arsenic is a chemical element that is toxic, and long-term exposure to it causes cancers such as lung, skin, liver, and bladder cancers. Over 150 million people around the world are affected by arsenic exposure. However, the molecular mechanism of how arsenic induces carcinogenesis is still not clear. As a carcinogen, arsenic has been demonstrated not to cause point mutations. Hence, the understanding of the dysregulation of epigenetic mechanisms caused by arsenic may help to unravel the mechanisms by which arsenic induces cancers. Arsenic is a crucial environmental metalloid whose high toxicity levels negatively impact human health. It poses significant health concerns to millions of people in developed and developing countries such as the USA, Canada, Bangladesh, India, China, and Mexico by enhancing sensitivity to various types of diseases, including cancers. However, how arsenic causes changes in gene expression that results in heinous conditions remains elusive. One of the proposed essential mechanisms that still has seen limited research with regard to causing disease upon arsenic exposure is the dysregulation of epigenetic components. In this review, we have extensively summarized current discoveries in arsenic-induced epigenetic modifications in carcinogenesis and angiogenesis. Importantly, we highlight the possible mechanisms underlying epigenetic reprogramming through arsenic exposure that cause changes in cell signaling and dysfunctions of different epigenetic elements.