{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kaushal JB"],"funding":["United States Department of Defense | United States Army | Army Medical Command | Congressionally Directed Medical Research Programs","United States Department of Defense | United States Army | Army Medical Command | Congressionally Directed Medical Research Programs (CDMRP)"],"pagination":["1007-1023"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11976299"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["44(15)"],"pubmed_abstract":["The functional activation of the androgen receptor (AR) and its interplay with the aberrant Hh/Gli cascade are pivotal in the progression of castration-resistant prostate cancer (CRPC) and resistance to AR-targeted therapies. Our study unveiled a novel role of the truncated form of Gli (t-Gli3) in advancing CRPC. Investigation into Gli3 regulation revealed a Smo-independent mechanism for its activation. Despite lacking a transactivation domain, t-Gli3 relies on androgen receptor variant 7 (AR-V7) for its action. Mechanistically, Gsk3β activation led to the t-Gli3 generation, and inhibition of Gsk3β supported the accumulation of full-length Gli3 expression through a non-canonical mechanism. Knockdown of Gsk3β (Gsk3β KD) reduces CRPC cell proliferation, induces apoptosis via mitochondrial fr"],"journal":["Oncogene"],"pubmed_title":["Oncogenic potential of truncated-Gli3 via the Gsk3β/Gli3/AR-V7 axis in castration-resistant prostate cancer."],"pmcid":["PMC11976299"],"funding_grant_id":["DOD W81XWH-18-1-0308","DOD W81XWH-21-1-0340","W81XWH-21-1-0640"],"pubmed_authors":["Parte S","Kaushal JB","Raut P","Sharma G","Seshacharyulu P","Lele SM","Batra SK","Halder S","Siddiqui JA","Alsafwani ZW","Abdullah KM"],"additional_accession":[]},"is_claimable":false,"name":"Oncogenic potential of truncated-Gli3 via the Gsk3β/Gli3/AR-V7 axis in castration-resistant prostate cancer.","description":"The functional activation of the androgen receptor (AR) and its interplay with the aberrant Hh/Gli cascade are pivotal in the progression of castration-resistant prostate cancer (CRPC) and resistance to AR-targeted therapies. Our study unveiled a novel role of the truncated form of Gli (t-Gli3) in advancing CRPC. Investigation into Gli3 regulation revealed a Smo-independent mechanism for its activation. Despite lacking a transactivation domain, t-Gli3 relies on androgen receptor variant 7 (AR-V7) for its action. Mechanistically, Gsk3β activation led to the t-Gli3 generation, and inhibition of Gsk3β supported the accumulation of full-length Gli3 expression through a non-canonical mechanism. Knockdown of Gsk3β (Gsk3β KD) reduces CRPC cell proliferation, induces apoptosis via mitochondrial fr","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2025-07-05T03:04:32.151Z","creation":"2025-07-05T03:04:32.151Z"},"accession":"S-EPMC11976299","cross_references":{"pubmed":["39821099"],"doi":["10.1038/s41388-024-03266-z"]}}