{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Varga A"],"funding":["National Research, Development and Innovation Office"],"pagination":["212"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9857065"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(2)"],"pubmed_abstract":["Prostate cancer metastasis is a significant cause of mortality in men. PKD3 facilitates tumor growth and metastasis, however, its regulation is largely unclear. The Hsp90 chaperone stabilizes an array of signaling client proteins, thus is an enabler of the malignant phenotype. Here, using different prostate cancer cell lines, we report that Hsp90 ensures PKD3 conformational stability and function to promote cancer cell migration. We found that pharmacological inhibition of either PKDs or Hsp90 dose-dependently abrogated the migration of DU145 and PC3 metastatic prostate cancer cells. Hsp90 inhibition by ganetespib caused a dose-dependent depletion of PKD2, PKD3, and Akt, which are all involved in metastasis formation. Proximity ligation assay and immunoprecipitation experiments demonstrate"],"journal":["Cells"],"pubmed_title":["Protein Kinase D3 (PKD3) Requires Hsp90 for Stability and Promotion of Prostate Cancer Cell Migration."],"pmcid":["PMC9857065"],"funding_grant_id":["TKP2021-EGA-24","K-131458","K-116525","K-124813"],"pubmed_authors":["Soti C","Muranyi J","Vantus T","Gyulavari P","Penzes K","Varga A","Csermely P","Nguyen MT","Gurbi B","Csala M","Batai B"],"additional_accession":[]},"is_claimable":false,"name":"Protein Kinase D3 (PKD3) Requires Hsp90 for Stability and Promotion of Prostate Cancer Cell Migration.","description":"Prostate cancer metastasis is a significant cause of mortality in men. PKD3 facilitates tumor growth and metastasis, however, its regulation is largely unclear. The Hsp90 chaperone stabilizes an array of signaling client proteins, thus is an enabler of the malignant phenotype. Here, using different prostate cancer cell lines, we report that Hsp90 ensures PKD3 conformational stability and function to promote cancer cell migration. We found that pharmacological inhibition of either PKDs or Hsp90 dose-dependently abrogated the migration of DU145 and PC3 metastatic prostate cancer cells. Hsp90 inhibition by ganetespib caused a dose-dependent depletion of PKD2, PKD3, and Akt, which are all involved in metastasis formation. Proximity ligation assay and immunoprecipitation experiments demonstrate","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-04T14:27:14.095Z","creation":"2025-04-04T14:27:14.095Z"},"accession":"S-EPMC9857065","cross_references":{"pubmed":["36672148"],"doi":["10.3390/cells12020212"]}}