Abstract
Arsenic is a ubiquitous metalloid whose high levels of toxicity pose major health concerns to millions of people worldwide by increasing susceptibility to various cancers and non-cancer illnesses. Since arsenic is not a mutagen, the mechanism by which it causes changes in gene expression and disease pathogenesis is not clear. One possible mechanism is through generation of reactive oxygen species. Another equally important mechanism still very much in its infancy is epigenetic dysregulation. In this review, we discuss recent discoveries underlying arsenic-induced epigenetic changes in cancer development. Importantly, we highlight the proposed mechanisms targeted by arsenic to drive oncogenic gene expression.
Original language | English |
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Pages (from-to) | 195-205 |
Number of pages | 11 |
Journal | Seminars in Cancer Biology |
Volume | 76 |
DOIs | |
State | Published - Nov 2021 |
Bibliographical note
Publisher Copyright:© 2021 Elsevier Ltd
Funding
This work was supported by National Institute of Environmental Health Sciences (NIEHS) grants R01ES030233 and 1R01ES024478 (YNF-M).
Funders | Funder number |
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National Institute of Environmental Health Sciences (NIEHS) | R01ES024478, R01ES030233 |
Keywords
- Alternative splicing
- Carcinogen
- DNA methylation
- Epigenetics
- Heavy metal
- Inorganic arsenic
- Transcription
ASJC Scopus subject areas
- Cancer Research