{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ehsani M"],"funding":["Deutsche Krebshilfe"],"pagination":["3263-3277"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9166678"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["41(23)"],"pubmed_abstract":["Castration-resistant prostate cancer (CRPC) is an aggressive lethal form of prostate cancer (PCa). Atraric acid (AA) not only inhibits the wild-type androgen receptor (AR) but also those AR mutants that confer therapy resistance to other clinically used AR antagonists, indicating a different mode of AR antagonism. AA induces cellular senescence and inhibits CRPC tumour growth in in vivo xenograft mouse model associated with reduced neo-angiogenesis suggesting the repression of intratumoural neo-angiogenesis by AA. In line with this, the secretome of CRPC cells mediates neo-angiogenesis in an androgen-dependent manner, which is counteracted by AA. This was confirmed by two in vitro models using primary human endothelial cells. Transcriptome sequencing revealed upregulated angiogenic pathway"],"journal":["Oncogene"],"pubmed_title":["The natural compound atraric acid suppresses androgen-regulated neo-angiogenesis of castration-resistant prostate cancer through angiopoietin 2."],"pmcid":["PMC9166678"],"funding_grant_id":["70113814"],"pubmed_authors":["Kotolloshi R","Mosig AS","Adam L","Neubert L","Ori A","Neri F","Huettner SS","Pungsrinont T","Rasa SMM","Ahmad A","Schindler K","Bartsch S","Berndt A","Ehsani M","Dittmann J","Grimm MO","Baniahmad A"],"additional_accession":[]},"is_claimable":false,"name":"The natural compound atraric acid suppresses androgen-regulated neo-angiogenesis of castration-resistant prostate cancer through angiopoietin 2.","description":"Castration-resistant prostate cancer (CRPC) is an aggressive lethal form of prostate cancer (PCa). Atraric acid (AA) not only inhibits the wild-type androgen receptor (AR) but also those AR mutants that confer therapy resistance to other clinically used AR antagonists, indicating a different mode of AR antagonism. AA induces cellular senescence and inhibits CRPC tumour growth in in vivo xenograft mouse model associated with reduced neo-angiogenesis suggesting the repression of intratumoural neo-angiogenesis by AA. In line with this, the secretome of CRPC cells mediates neo-angiogenesis in an androgen-dependent manner, which is counteracted by AA. This was confirmed by two in vitro models using primary human endothelial cells. Transcriptome sequencing revealed upregulated angiogenic pathway","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jun","modification":"2026-05-06T03:13:10.169Z","creation":"2024-11-09T00:02:30.467Z"},"accession":"S-EPMC9166678","cross_references":{"pubmed":["35513564"],"doi":["10.1038/s41388-022-02333-7"]}}