Vlahopoulos, S.; Pan, L.; Varisli, L.; Dancik, G.M.; Karantanos, T.; Boldogh, I. OGG1 as an Epigenetic Reader Affects NFκB: What This Means for Cancer. Cancers2024, 16, 148.
Vlahopoulos, S.; Pan, L.; Varisli, L.; Dancik, G.M.; Karantanos, T.; Boldogh, I. OGG1 as an Epigenetic Reader Affects NFκB: What This Means for Cancer. Cancers 2024, 16, 148.
Vlahopoulos, S.; Pan, L.; Varisli, L.; Dancik, G.M.; Karantanos, T.; Boldogh, I. OGG1 as an Epigenetic Reader Affects NFκB: What This Means for Cancer. Cancers2024, 16, 148.
Vlahopoulos, S.; Pan, L.; Varisli, L.; Dancik, G.M.; Karantanos, T.; Boldogh, I. OGG1 as an Epigenetic Reader Affects NFκB: What This Means for Cancer. Cancers 2024, 16, 148.
Abstract
8-oxoguanine glycosylase 1 (OGG1), which was initially identified as the enzyme that catalyzes the first step in the DNA base excision repair pathway, is now known also as a modulator of gene expression. What is important for cancer, is that OGG1 acts as a modulator of NFκB-driven gene expression. Specifically, oxidant stress in the cell transiently halts the enzymatic activity of substrate-bound OGG1. The stalled OGG1 facilitates DNA binding of transactivators, including NFκB, to their cognate sites to enable expression of cytokines and chemokines, with ensuing recruitment of inflammatory cells. Recently, we highlighted chief aspects of OGG1 involvement in regulation of gene expression, which have a significance in lung cancer development. However, OGG1 has also been implicated in the molecular underpinning of acute myeloid leukemia. In general, the capacity of cancer cells to adapt to oxidative stress depends on molecular systems such as the interface of OGG1 with NFκB, which bestows a cancer cell with the molecular mechanism of transformation of its microenvironment to enable adaptation and survival of malignant clones.
Biology and Life Sciences, Biochemistry and Molecular Biology
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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