{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Warren AY"],"funding":["Cancer Research UK","Prostate Cancer UK","NCI NIH HHS"],"pagination":["1136-1150"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6514849"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["38(7)"],"pubmed_abstract":["Elucidation of mechanisms underlying the increased androgen receptor (AR) activity and subsequent development of aggressive prostate cancer (PrCa) is pivotal in developing new therapies. Using a systems biology approach, we interrogated the AR-regulated proteome and identified PDZ binding kinase (PBK) as a novel AR-regulated protein that regulates full-length AR and AR variants (ARVs) activity in PrCa. PBK overexpression in aggressive PrCa is associated with early biochemical relapse and poor clinical outcome. In addition to its carboxy terminus ligand-binding domain, PBK directly interacts with the amino terminus transactivation domain of the AR to stabilise it thereby leading to increased AR protein expression observed in PrCa. Transcriptome sequencing revealed that PBK is a mediator of "],"journal":["Oncogene"],"pubmed_title":["A reciprocal feedback between the PDZ binding kinase and androgen receptor drives prostate cancer."],"pmcid":["PMC6514849"],"funding_grant_id":["R01 CA174777","20411","S10-10","22310"],"pubmed_authors":["Warren AY","Tilley WD","Zhao W","Escriu C","Zecchini VR","Mohammed H","Qureshi A","Shaw GL","Selth LA","Menon S","Asim M","Massie CE","Watt K","Neal DE","Carroll JS","Taylor C","D'Santos C","Luko K","Pungsrinont T","Yang X","Orafidiya F","Baridi A","Dehm SM","Mills IG","McEwan IJ","Chohan BS","Baniahmad A"],"additional_accession":[]},"is_claimable":false,"name":"A reciprocal feedback between the PDZ binding kinase and androgen receptor drives prostate cancer.","description":"Elucidation of mechanisms underlying the increased androgen receptor (AR) activity and subsequent development of aggressive prostate cancer (PrCa) is pivotal in developing new therapies. Using a systems biology approach, we interrogated the AR-regulated proteome and identified PDZ binding kinase (PBK) as a novel AR-regulated protein that regulates full-length AR and AR variants (ARVs) activity in PrCa. PBK overexpression in aggressive PrCa is associated with early biochemical relapse and poor clinical outcome. In addition to its carboxy terminus ligand-binding domain, PBK directly interacts with the amino terminus transactivation domain of the AR to stabilise it thereby leading to increased AR protein expression observed in PrCa. Transcriptome sequencing revealed that PBK is a mediator of ","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Feb","modification":"2026-05-07T04:35:03.585Z","creation":"2019-07-25T07:16:13Z"},"accession":"S-EPMC6514849","cross_references":{"pubmed":["30237440"],"doi":["10.1038/s41388-018-0501-z"]}}