{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["136(2)"],"submitter":["Feng T"],"pubmed_abstract":["Androgen deprivation therapy is the primary treatment for advanced prostate tumors. While initially effective, tumor progression to the therapy-resistant stage is inevitable. Paradoxically, UDP glucuronosyltransferase family 2 member B17 (UGT2B17), the key enzyme responsible for androgen catabolism in prostate tumor cells, is upregulated in therapy-resistant tumors, though its role in tumor progression remains unclear. Here, we demonstrate that UGT2B17 possesses multiple oncogenic functions independent of androgen catabolism. It modulates protein-folding pathways, allowing tumor cells to endure therapy-induced stress. UGT2B17 also regulates transcription associated with cell division and the DNA damage response, enabling unchecked cell proliferation. Targeting the newly identified UGT2B17 "],"journal":["The Journal of clinical investigation"],"pagination":["e196495"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12807465"],"repository":["biostudies-literature"],"pubmed_title":["Noncanonical functions of UGT2B17 promote castration-resistant prostate cancer progression."],"pmcid":["PMC12807465"],"pubmed_authors":["Levesque E","Qi J","Kung SH","Dong X","Xie N","Fazli L","Wang L","Jia Q","Li Y","Han B","Lack NA","Gao L","Morova T","Lacombe L","Guillemette C","Feng T"],"additional_accession":[]},"is_claimable":false,"name":"Noncanonical functions of UGT2B17 promote castration-resistant prostate cancer progression.","description":"Androgen deprivation therapy is the primary treatment for advanced prostate tumors. While initially effective, tumor progression to the therapy-resistant stage is inevitable. Paradoxically, UDP glucuronosyltransferase family 2 member B17 (UGT2B17), the key enzyme responsible for androgen catabolism in prostate tumor cells, is upregulated in therapy-resistant tumors, though its role in tumor progression remains unclear. Here, we demonstrate that UGT2B17 possesses multiple oncogenic functions independent of androgen catabolism. It modulates protein-folding pathways, allowing tumor cells to endure therapy-induced stress. UGT2B17 also regulates transcription associated with cell division and the DNA damage response, enabling unchecked cell proliferation. Targeting the newly identified UGT2B17 ","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-06-10T05:13:29.153Z","creation":"2026-06-10T03:07:44.122Z"},"accession":"S-EPMC12807465","cross_references":{"pubmed":["41343245"],"doi":["10.1172/JCI196495"]}}