Arsenic co-carcinogenesis: Inhibition of DNA repair and interaction with zinc finger proteins

• Published in: Seminars in cancer biology Vol. 76; pp. 86 - 98
• Main Authors: Zhou, Xixi, Speer, Rachel M., Volk, Lindsay, Hudson, Laurie G., Liu, Ke Jian
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.11.2021
• Subjects: Animals; Arsenic; Arsenic - adverse effects; Co-carcinogenesis; Cocarcinogenesis - metabolism; Cocarcinogenesis - pathology; DNA repair; DNA Repair - drug effects; DNA Repair - physiology; Humans; ROS; Zinc finger; Zinc Fingers - drug effects; PTPs; PCNA; Arsenic; H3K9me2; mtDNA; DNA repair; EGFR; H3K36me3; BaP; BPDE; UVR; DNMT; RNS; Zinc finger; AsIII; 8-OHdG; WHO; SS; HEKn; MMAIII; GST; IR; SOD; PARP-1; SOH; BER; GPx; Co-carcinogenesis; MMR; NOS; CPD; NOX; 6-4 PPs; EPA; ROS; PAHs; NER; ATO; DSBR
• ISSN: 1044-579X; 1096-3650
• DOI: 10.1016/j.semcancer.2021.05.009

Arsenic is widely present in the environment and is associated with various population health risks including cancers. Arsenic exposure at environmentally relevant levels enhances the mutagenic effect of other carcinogens such as ultraviolet radiation. Investigation on the molecular mechanisms could inform the prevention and intervention strategies of arsenic carcinogenesis and co-carcinogenesis. Arsenic inhibition of DNA repair has been demonstrated to be an important mechanism, and certain DNA repair proteins have been identified to be extremely sensitive to arsenic exposure. This review will summarize the recent advances in understanding the mechanisms of arsenic carcinogenesis and co-carcinogenesis, including DNA damage induction and ROS generation, particularly how arsenic inhibits DNA repair through an integrated molecular mechanism which includes its interactions with sensitive zinc finger DNA repair proteins.