{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Al-Nakouzi N"],"funding":["Gouvernement du Canada | Instituts de Recherche en Santé du Canada | CIHR Skin Research Training Centre","NCI NIH HHS","Mitacs","Prostate Cancer Canada","CIHR"],"pagination":["4760"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9376089"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Lineage plasticity of prostate cancer is associated with resistance to androgen receptor (AR) pathway inhibition (ARPI) and supported by a reactive tumor microenvironment. Here we show that changes in chondroitin sulfate (CS), a major glycosaminoglycan component of the tumor cell glycocalyx and extracellular matrix, is AR-regulated and promotes the adaptive progression of castration-resistant prostate cancer (CRPC) after ARPI. AR directly represses transcription of the 4-O-sulfotransferase gene CHST11 under basal androgen conditions, maintaining steady-state CS in prostate adenocarcinomas. When AR signaling is inhibited by ARPI or lost during progression to non-AR-driven CRPC as a consequence of lineage plasticity, CHST11 expression is unleashed, leading to elevated 4-O-sulfated chondroiti"],"journal":["Nature communications"],"pubmed_title":["Reformation of the chondroitin sulfate glycocalyx enables progression of AR-independent prostate cancer."],"pmcid":["PMC9376089"],"funding_grant_id":["RS2014-02","IT06057","PJT-153092","P50 CA097186"],"pubmed_authors":["Al-Nakouzi N","Wang CK","Esko JD","Fazli L","Adomat H","Esfandnia S","Gustavsson T","Clausen TM","Nelson PS","Wang Y","Corey E","Daugaard M","Lallous N","Lo J","Gleave ME","Salanti A","Hui D","Khazamipour N","Dagil R","Chauchereau A","Collins C","Choudhary S","Truong S","Spliid CB","Oo HZ","Nelepcu I"],"additional_accession":[]},"is_claimable":false,"name":"Reformation of the chondroitin sulfate glycocalyx enables progression of AR-independent prostate cancer.","description":"Lineage plasticity of prostate cancer is associated with resistance to androgen receptor (AR) pathway inhibition (ARPI) and supported by a reactive tumor microenvironment. Here we show that changes in chondroitin sulfate (CS), a major glycosaminoglycan component of the tumor cell glycocalyx and extracellular matrix, is AR-regulated and promotes the adaptive progression of castration-resistant prostate cancer (CRPC) after ARPI. AR directly represses transcription of the 4-O-sulfotransferase gene CHST11 under basal androgen conditions, maintaining steady-state CS in prostate adenocarcinomas. When AR signaling is inhibited by ARPI or lost during progression to non-AR-driven CRPC as a consequence of lineage plasticity, CHST11 expression is unleashed, leading to elevated 4-O-sulfated chondroiti","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2026-05-09T14:09:07.51Z","creation":"2025-04-04T08:01:40.652Z"},"accession":"S-EPMC9376089","cross_references":{"pubmed":["35963852"],"doi":["10.1038/s41467-022-32530-7"]}}