{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mirzakhani K"],"funding":["Deutsche Krebshilfe"],"pagination":["943-959"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8837536"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["41(7)"],"pubmed_abstract":["The bipolar androgen therapy (BAT) to treat prostate cancer (PCa) includes cycles of supraphysiological androgen levels (SAL) under androgen-deprivation therapy (ADT). We showed previously that SAL induces cellular senescence in androgen-sensitive PCa cells and in ex vivo-treated patient PCa tumor samples. Here, we analyzed the underlying molecular pathway and reveal that SAL induces cellular senescence in both, castration-sensitive (CSPC) LNCaP and castration-resistant PCa (CRPC) C4-2 cells through the cell cycle inhibitor p15<sup>INK4b</sup> and increased phosphorylation of AKT. Treatment with the AKT inhibitor (AKTi) potently inhibited SAL-induced expression of p15<sup>INK4b</sup> and cellular senescence in both cell lines. Proximity-ligation assays (PLA) combined with high-resolution l"],"journal":["Oncogene"],"pubmed_title":["The androgen receptor-lncRNASAT1-AKT-p15 axis mediates androgen-induced cellular senescence in prostate cancer cells."],"pmcid":["PMC8837536"],"funding_grant_id":["70113814"],"pubmed_authors":["Rasa SMM","Mirzakhani K","Gassler N","Ehsani M","Leeder M","Neri F","Ungelenk M","Grimm MO","Kallenbach J","Ribaudo F","Gong W","Baniahmad A"],"additional_accession":[]},"is_claimable":false,"name":"The androgen receptor-lncRNASAT1-AKT-p15 axis mediates androgen-induced cellular senescence in prostate cancer cells.","description":"The bipolar androgen therapy (BAT) to treat prostate cancer (PCa) includes cycles of supraphysiological androgen levels (SAL) under androgen-deprivation therapy (ADT). We showed previously that SAL induces cellular senescence in androgen-sensitive PCa cells and in ex vivo-treated patient PCa tumor samples. Here, we analyzed the underlying molecular pathway and reveal that SAL induces cellular senescence in both, castration-sensitive (CSPC) LNCaP and castration-resistant PCa (CRPC) C4-2 cells through the cell cycle inhibitor p15<sup>INK4b</sup> and increased phosphorylation of AKT. Treatment with the AKT inhibitor (AKTi) potently inhibited SAL-induced expression of p15<sup>INK4b</sup> and cellular senescence in both cell lines. Proximity-ligation assays (PLA) combined with high-resolution l","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2025-04-04T13:21:29.719Z","creation":"2025-04-04T13:21:29.719Z"},"accession":"S-EPMC8837536","cross_references":{"pubmed":["34667276"],"doi":["10.1038/s41388-021-02060-5"]}}