| Role of protein kinase C-iota in transformed non-malignant RWPE-1 cells and androgen-independent prostate carcinoma DU-145 cells. | |
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MedLine Citation:
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PMID: 19243387 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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MATERIALS AND METHODS: Western blotting and immunoprecipitations demonstrated that PKC-iotaisassociated with cyclin-dependent kinase activating kinase (CAK/Cdk7) in RWPE-1 cells, but not in DU-145 cells. RESULTS: Treatment of prostate RWPE-1 cells with PKC-iota silencing RNA (siRNA) decreased cell viability,cell-cycle accumulation at G2/M phase, and phosphorylation of Cdk7 and Cdk2. In addition, PKC-iota siRNA treatment caused less phosphorylation ofBad at ser-155, ser-136, and greater Bad/Bcl-xL heterodimerization, leading to apoptosis. In DU-145 cells, PKC-iota was anti-apoptotic and was required for cell survival. Treatment with PKC-iota siRNA blocked increase in cell number, and inhibited G1/S transition by accumulation of cells in G0/G1phase. In addition to cell-cycle arrest, both RWPE-1 and DU-145 cells underwent apoptosis due to mitochondrial dysfunction and apoptosis cascades, such as release of cytochrome c,activation of caspase-7, and poly (ADP-ribose)polymerase (PARP) cleavage. CONCLUSION: Our results suggest that PKC-iota is required for cell survival in both transformed non-malignant prostate RWPE-1 cells and androgen-independent malignant prostate DU-145 cells, whereas suppressing PKC-iota lead to apoptosis in DU-145 prostate cells. |
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Authors:
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H Y Win; M Acevedo-Duncan |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Cell proliferation Volume: 42 ISSN: 1365-2184 ISO Abbreviation: Cell Prolif. Publication Date: 2009 Apr |
Date Detail:
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Created Date: 2009-03-26 Completed Date: 2009-04-16 Revised Date: 2012-06-13 |
Medline Journal Info:
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Nlm Unique ID: 9105195 Medline TA: Cell Prolif Country: England |
Other Details:
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Languages: eng Pagination: 182-94 Citation Subset: IM |
Affiliation:
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Department of Chemistry, University of South Florida, Tampa, Florida, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis
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physiology Cell Count Cell Cycle / physiology Cell Line, Transformed Cell Line, Tumor Cell Survival / physiology Cyclin-Dependent Kinase 2 / metabolism Cyclin-Dependent Kinases / metabolism Humans Isoenzymes / metabolism, physiology* Male Phosphorylation Poly(ADP-ribose) Polymerases / metabolism Prostate / enzymology, metabolism*, pathology Prostatic Neoplasms / enzymology, metabolism*, pathology Protein Kinase C / metabolism, physiology* RNA, Small Interfering / genetics bcl-Associated Death Protein / metabolism bcl-X Protein / metabolism |
| Chemical | |
Reg. No./Substance:
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0/BAD protein, human; 0/BCL2L1 protein, human; 0/Isoenzymes; 0/RNA, Small Interfering; 0/bcl-Associated Death Protein; 0/bcl-X Protein; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 2.7.11.13/Protein Kinase C; EC 2.7.11.13/protein kinase C lambda; EC 2.7.11.22/Cyclin-Dependent Kinase 2; EC 2.7.11.22/Cyclin-Dependent Kinases; EC 2.7.11.22/cyclin-dependent kinase-activating kinase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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