Site-specific decreases in DNA methylation in replicating cells following exposure to oxidative stress.

ABSTRACT: Oxidative stress is a common feature of inflammation-driven cancers, and it promotes genomic instability and aggressive tumour phenotypes. It is known that oxidative stress transiently modulates gene expression through the oxidation of transcription factors and associated regulatory proteins. Neutrophils are our most abundant white blood cells and accumulate at sites of infection and inflammation. Activated neutrophils produce hypochlorous acid and chloramines, which can disrupt DNA methylation by oxidizing methionine. The goal of the current study was to determine whether chloramine exposure results in sequence-specific modifications in DNA methylation that enable long-term alterations in transcriptional output. Proliferating Jurkat T-lymphoma cells were exposed to sublethal doses of glyc

SUBMITTER: Seddon AR 

PROVIDER: S-EPMC9896486 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature