Rakesh , Kumar (2020) A new insight into base excision repair (BER) in targeted cancer therapy. Genome Instability & Disease, 1. pp. 310-317. ISSN 2524-7662

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Abstract

Dysregulation of redox homeostasis and the resulting generation of excessive reactive oxygen species (ROS) and oxida-tive DNA damage play an obligatory role in the progression of human cancer as well as therapeutic sensitivity to a variety of genome-targeting cancer drugs. In a recent study, Bao et al. (Free Radic Biol Med, 2020), present a novel mechanism that governs the sensitivity of certain cancer cells to DNA damaging therapies. The authors have identified a novel, ROS-associated, lysine acetylation modification in Uracil-DNA N-glycosylase 2 (UNG2)—a key understudied component of the base excision repair pathway, which primes UNG2 for subsequent ubiquitination by UHRF1 ligase, leading to coupling the UNG2 degradation to cancer cell death in a ROS-sensitive manner. Translational innovation of these mechanistic findings resides by the ability of epigenetic therapeutic inhibitors to elevate the levels of UNG2-Lys78 acetylation, leading to sensitiz-ing ROS-resistant cancer cells to DNA damaging therapeutic agents. I close this commentary by briefly summarizing some outstanding questions and postulations in the field in the context of the novel findings presented by Bao et a

Item Type:	Article
Uncontrolled Keywords:	DNA damaging therapies · BER · UNG2 · Therapeutic resistance · ROS biology · Epigenetic combination therapy
Subjects:	Cancer Research
Depositing User:	Central Library RGCB
Date Deposited:	28 Jan 2021 07:03
Last Modified:	28 Jan 2021 07:03
URI:	http://rgcb.sciencecentral.in/id/eprint/1017

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