{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yoshihama Y"],"funding":["HHS | National Institutes of Health","UT | University of Texas MD Anderson Cancer Center","Prostate Cancer Foundation"],"pagination":["e2026324118"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8433584"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["118(36)"],"pubmed_abstract":["Prostate cancer is a leading cause of cancer-related mortality in men. The widespread use of androgen receptor (AR) inhibitors has generated an increased incidence of AR-negative prostate cancer, triggering the need for effective therapies for such patients. Here, analysis of public genome-wide CRISPR screens in human prostate cancer cell lines identified histone demethylase JMJD1C (KDM3C) as an AR-negative context-specific vulnerability. Secondary validation studies in multiple cell lines and organoids, including isogenic models, confirmed that small hairpin RNA (shRNA)-mediated depletion of JMJD1C potently inhibited growth specifically in AR-negative prostate cancer cells. To explore the cooperative interactions of AR and JMJD1C, we performed comparative transcriptomics of 1) isogenic AR"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["AR-negative prostate cancer is vulnerable to loss of JMJD1C demethylase."],"pmcid":["PMC8433584"],"funding_grant_id":["R01 CA231349-01A1","R35 GM130119","17CHAL17","Prostate Cancer Moon Shot"],"pubmed_authors":["Li J","Wang YA","LaBella KA","Yoshihama Y","Kim E","Wu CJ","Hart T","Colic M","Shang X","DePinho RA","Spring DJ","Bertolet L"],"additional_accession":[]},"is_claimable":false,"name":"AR-negative prostate cancer is vulnerable to loss of JMJD1C demethylase.","description":"Prostate cancer is a leading cause of cancer-related mortality in men. The widespread use of androgen receptor (AR) inhibitors has generated an increased incidence of AR-negative prostate cancer, triggering the need for effective therapies for such patients. Here, analysis of public genome-wide CRISPR screens in human prostate cancer cell lines identified histone demethylase JMJD1C (KDM3C) as an AR-negative context-specific vulnerability. Secondary validation studies in multiple cell lines and organoids, including isogenic models, confirmed that small hairpin RNA (shRNA)-mediated depletion of JMJD1C potently inhibited growth specifically in AR-negative prostate cancer cells. To explore the cooperative interactions of AR and JMJD1C, we performed comparative transcriptomics of 1) isogenic AR","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2025-04-05T14:05:21.447Z","creation":"2025-04-05T14:05:21.447Z"},"accession":"S-EPMC8433584","cross_references":{"pubmed":["34475205"],"doi":["10.1073/pnas.2026324118"]}}