{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen M"],"funding":["Universidade de Macau"],"pagination":["e53468"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9346471"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(8)"],"pubmed_abstract":["Androgen receptor (AR) is a master transcription factor that drives prostate cancer (PCa) development and progression. Alterations in the expression or activity of AR coregulators significantly impact the outcome of the disease. Using a proteomics approach, we identified the tripartite motif-containing 33 (TRIM33) as a novel transcriptional coactivator of AR. We demonstrate that TRIM33 facilitates AR chromatin binding to directly regulate a transcription program that promotes PCa progression. TRIM33 further stabilizes AR by protecting it from Skp2-mediated ubiquitination and proteasomal degradation. We also show that TRIM33 is essential for PCa tumor growth by avoiding cell-cycle arrest and apoptosis, and TRIM33 knockdown sensitizes PCa cells to AR antagonists. In clinical analyses, we fin"],"journal":["EMBO reports"],"pubmed_title":["TRIM33 drives prostate tumor growth by stabilizing androgen receptor from Skp2-mediated degradation."],"pmcid":["PMC9346471"],"funding_grant_id":["MYRG2020‐00100‐FHS","MYRG2018‐00033‐FHS"],"pubmed_authors":["Narwade N","Zheng Y","Tang AHN","Lei KMK","Chen M","Cheung E","Lingadahalli S","Liu S","Zhao Z","Lu Q","Poon TCW"],"additional_accession":[]},"is_claimable":false,"name":"TRIM33 drives prostate tumor growth by stabilizing androgen receptor from Skp2-mediated degradation.","description":"Androgen receptor (AR) is a master transcription factor that drives prostate cancer (PCa) development and progression. Alterations in the expression or activity of AR coregulators significantly impact the outcome of the disease. Using a proteomics approach, we identified the tripartite motif-containing 33 (TRIM33) as a novel transcriptional coactivator of AR. We demonstrate that TRIM33 facilitates AR chromatin binding to directly regulate a transcription program that promotes PCa progression. TRIM33 further stabilizes AR by protecting it from Skp2-mediated ubiquitination and proteasomal degradation. We also show that TRIM33 is essential for PCa tumor growth by avoiding cell-cycle arrest and apoptosis, and TRIM33 knockdown sensitizes PCa cells to AR antagonists. In clinical analyses, we fin","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2026-07-14T16:42:17.671Z","creation":"2025-04-21T22:12:29.063Z"},"accession":"S-EPMC9346471","cross_references":{"pubmed":["35785414"],"doi":["10.15252/embr.202153468"]}}