Document Detail


Role of protein kinase C-iota in transformed non-malignant RWPE-1 cells and androgen-independent prostate carcinoma DU-145 cells.
MedLine Citation:
PMID:  19243387     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
H Y Win; M Acevedo-Duncan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cell proliferation     Volume:  42     ISSN:  1365-2184     ISO Abbreviation:  Cell Prolif.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-03-26     Completed Date:  2009-04-16     Revised Date:  2012-06-13    
Medline Journal Info:
Nlm Unique ID:  9105195     Medline TA:  Cell Prolif     Country:  England    
Other Details:
Languages:  eng     Pagination:  182-94     Citation Subset:  IM    
Affiliation:
Department of Chemistry, University of South Florida, Tampa, Florida, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / 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:
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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