title: Decoding the histone code: Role of H3K36me3 in mismatch repair and implications for cancer susceptibility and therapy.
abstract: DNA mismatch repair (MMR) maintains genome stability primarily by correcting replication-associated mismatches. Defects in MMR lead to several human cancers characterized by frequent alterations in simple repetitive DNA sequences, a phenomenon called microsatellite instability (MSI). In most MSI-positive cancers, genetic or epigenetic changes that alter the function or expression of an essential MMR protein have been identified. However, in a subset of MSI-positive cancers, epigenetic or genetic changes have not been found in known MMR genes, such that the molecular basis of the MMR defect in these cells remains unknown. A possible answer to this puzzle emerged recently when it was discovered that H3K36me3, a well-studied posttranslational histone modification or histone mark, plays a role in regulating human MMR in vivo. In this review, potential roles for this histone mark to modulate genome stability and cancer susceptibility in human cells are discussed.
authors.affiliation: Author's Affiliations: Graduate Center for Toxicology, Markey Cancer Center, University of Kentucky College of Medicine, Lexington, Kentucky; and Tsinghua University School of Medicine, Beijing, China.
authors.forename: Guo-Min
authors.initials: GM
authors.lastname: Li
mesh_terms: D020137:Base Pair Mismatch / Q000235:genetics*; D042421:Histone Code; D006801:Humans; D008239:Lysine / Q000378:metabolism*; D008745:Methylation; D009369:Neoplasms / Q000209:etiology* / Q000628:therapy*; D063151:Polycomb Repressive Complex 2 / Q000378:metabolism*
chemical_list: D063151:Polycomb Repressive Complex 2; D008239:Lysine