{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Ahmad T"],"funding":["NCI NIH HHS"],"pubmed_abstract":["Chemoresistance remains a major obstacle to effective cancer treatment, often driven by enhanced DNA repair mechanisms that enable tumor cells to withstand genotoxic therapies. One such pathway involves the atypical DNA damage repair complex ALKBH3-ASCC, activated by the E3 ligase RNF113A in response to alkylation damage. We previously showed that SMYD3-dependent methylation of RNF113A stimulates this pathway, enhancing DNA repair and promoting resistance. Here, we identify KDM7B/PHF8 as the bona fide RNF113A demethylase, establishing one of the first functional examples of a dynamic, reversible non-histone methylation event regulating genome integrity. KDM7B antagonizes SMYD3 activity by maintaining low levels of methylated RNF113A, thereby limiting ASCC activation and sensitizing cancer "],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2026.01.03.697470"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12776375"],"repository":["biostudies-literature"],"pubmed_title":["KDM7B-mediated demethylation of RNF113A regulates small cell lung cancer sensitivity to alkylation damage."],"pmcid":["PMC12776375"],"funding_grant_id":["R01 CA278940","K99 CA255936","R01 CA236949","R01 CA272843","R01 CA266280","R01 CA272844"],"pubmed_authors":["Belmudes L","Coute Y","Tsao N","Lan F","Lu X","Ahmad T","Chasan T","Bhowmik MC","Hausmann S","Foucher AE","Dubiez E","Reynoird N","Yang X","Mazur PK","Ren L","Boussouar F","Flores N","Blanchet S","Wan J","Chuffart F","Kadlec J","Mosammaparast N","Vayr J"],"additional_accession":[]},"is_claimable":false,"name":"KDM7B-mediated demethylation of RNF113A regulates small cell lung cancer sensitivity to alkylation damage.","description":"Chemoresistance remains a major obstacle to effective cancer treatment, often driven by enhanced DNA repair mechanisms that enable tumor cells to withstand genotoxic therapies. One such pathway involves the atypical DNA damage repair complex ALKBH3-ASCC, activated by the E3 ligase RNF113A in response to alkylation damage. We previously showed that SMYD3-dependent methylation of RNF113A stimulates this pathway, enhancing DNA repair and promoting resistance. Here, we identify KDM7B/PHF8 as the bona fide RNF113A demethylase, establishing one of the first functional examples of a dynamic, reversible non-histone methylation event regulating genome integrity. KDM7B antagonizes SMYD3 activity by maintaining low levels of methylated RNF113A, thereby limiting ASCC activation and sensitizing cancer ","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-06-03T03:13:32.894Z","creation":"2026-06-03T03:10:31.261Z"},"accession":"S-EPMC12776375","cross_references":{"pubmed":["41509214"],"doi":["10.64898/2026.01.03.697470"]}}