{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu J"],"funding":["Fundamental Research Funds for the Central Universities","Research Fund of Zhongnan Hospital of Wuhan University","National Natural Science Foundation of China"],"pagination":["e2403995"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11615784"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(45)"],"pubmed_abstract":["Bladder cancer (BLCA) is a prevalent cancer with high case-fatality rates and a substantial economic burden worldwide. Understanding its molecular underpinnings to guide clinical management is crucial. Ferroptosis, a recently described non-apoptotic form of cell death, is initiated by the lethal accumulation of iron-dependent lipid peroxidation products. Despite growing interest, the roles and vulnerabilities determining ferroptosis sensitivity in BLCA remain unclear. Re-analysis of single-cell RNA data reveals a decrease in high-ferroptosis cancer cells as BLCA advances. USP52/PAN2 is identified as a key regulator of ferroptosis in BLCA through an unbiased siRNA screen targeting 96 deubiquitylases (DUBs). Functionally, USP52 depletion impedes glutathione (GSH) synthesis by promoting xCT p"],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["Deubiquitylase USP52 Promotes Bladder Cancer Progression by Modulating Ferroptosis through Stabilizing SLC7A11/xCT."],"pmcid":["PMC11615784"],"funding_grant_id":["YYXKNLJS2024001","82472733","PTPP2024001","RLYC2024001001","2042022dx0003","SWYBK01-03"],"pubmed_authors":["Liu J","Jin W","Xiao Y","Wang G","Yu J","Zhang R","Li M","Ju L","Jiang W","Zhang Y","Luo Y","Wei H","Zhou F","Wang X","Chen S","Wang Y","Qian K"],"additional_accession":[]},"is_claimable":false,"name":"Deubiquitylase USP52 Promotes Bladder Cancer Progression by Modulating Ferroptosis through Stabilizing SLC7A11/xCT.","description":"Bladder cancer (BLCA) is a prevalent cancer with high case-fatality rates and a substantial economic burden worldwide. Understanding its molecular underpinnings to guide clinical management is crucial. Ferroptosis, a recently described non-apoptotic form of cell death, is initiated by the lethal accumulation of iron-dependent lipid peroxidation products. Despite growing interest, the roles and vulnerabilities determining ferroptosis sensitivity in BLCA remain unclear. Re-analysis of single-cell RNA data reveals a decrease in high-ferroptosis cancer cells as BLCA advances. USP52/PAN2 is identified as a key regulator of ferroptosis in BLCA through an unbiased siRNA screen targeting 96 deubiquitylases (DUBs). Functionally, USP52 depletion impedes glutathione (GSH) synthesis by promoting xCT p","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Dec","modification":"2026-06-02T09:12:17.875Z","creation":"2025-04-06T17:33:34.808Z"},"accession":"S-EPMC11615784","cross_references":{"pubmed":["39392373"],"doi":["10.1002/advs.202403995"]}}