{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hoffmann MJ"],"funding":["Deutsche Forschungsgemeinschaft"],"pagination":["260"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7916885"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(2)"],"pubmed_abstract":["Since genes encoding epigenetic regulators are often mutated or deregulated in urothelial carcinoma (UC), they represent promising therapeutic targets. Specifically, inhibition of Class-I histone deacetylase (HDAC) isoenzymes induces cell death in UC cell lines (UCC) and, in contrast to other cancer types, cell cycle arrest in G2/M. Here, we investigated whether mutations in cell cycle genes contribute to G2/M rather than G1 arrest, identified the precise point of arrest and clarified the function of individual HDAC Class-I isoenzymes. Database analyses of UC tissues and cell lines revealed mutations in G1/S, but not G2/M checkpoint regulators. Using class I-specific HDAC inhibitors (HDACi) with different isoenzyme specificity (Romidepsin, Entinostat, RGFP966), cell cycle arrest was shown "],"journal":["Genes"],"pubmed_title":["Downregulation of Cell Cycle and Checkpoint Genes by Class I HDAC Inhibitors Limits Synergism with G2/M Checkpoint Inhibitor MK-1775 in Bladder Cancer Cells."],"pmcid":["PMC7916885"],"funding_grant_id":["HO 6448/ NI 1398"],"pubmed_authors":["Hommel K","Meneceur S","Schulz WA","Hoffmann MJ","Niegisch G"],"additional_accession":[]},"is_claimable":false,"name":"Downregulation of Cell Cycle and Checkpoint Genes by Class I HDAC Inhibitors Limits Synergism with G2/M Checkpoint Inhibitor MK-1775 in Bladder Cancer Cells.","description":"Since genes encoding epigenetic regulators are often mutated or deregulated in urothelial carcinoma (UC), they represent promising therapeutic targets. Specifically, inhibition of Class-I histone deacetylase (HDAC) isoenzymes induces cell death in UC cell lines (UCC) and, in contrast to other cancer types, cell cycle arrest in G2/M. Here, we investigated whether mutations in cell cycle genes contribute to G2/M rather than G1 arrest, identified the precise point of arrest and clarified the function of individual HDAC Class-I isoenzymes. Database analyses of UC tissues and cell lines revealed mutations in G1/S, but not G2/M checkpoint regulators. Using class I-specific HDAC inhibitors (HDACi) with different isoenzyme specificity (Romidepsin, Entinostat, RGFP966), cell cycle arrest was shown ","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Feb","modification":"2025-04-19T05:10:35.187Z","creation":"2021-03-03T08:14:22Z"},"accession":"S-EPMC7916885","cross_references":{"pubmed":["33670166"],"doi":["10.3390/genes12020260"]}}