Document Detail


Transgenic overexpression of PKCε in the mouse prostate induces preneoplastic lesions.
MedLine Citation:
PMID:  21224724     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
It is well established that protein kinase C (PKC) isozymes play distinctive roles in mitogenic and survival signaling as well as in cancer progression. PKCε, the product of the PRKCE gene, is up-regulated in various types of cancers including prostate, lung and breast cancer. To address a potential role for PKCs in prostate cancer progression we generated three mouse transgenic lines expressing PKCα, PKCδ, or PKCε in the prostate epithelium under the control of the rat probasin (PB) promoter. Whereas PB-PKCε and PB-PKCδ mice did not show any evident phenotype, PB-PKCε mice developed prostate hyperplasia as well as prostate intraepithelial neoplasia (PIN) that displayed enhanced phospho-Akt, phospho-S6, and phospho-Stat3 levels, as well as enhanced resistance to apoptotic stimuli. PKCε overexpression was insufficient to drive neoplastic changes in the mouse prostate. Notably, overexpression of PKCε by adenoviral means in normal immortalized RWPE-1 prostate cells confers a growth advantage and hyperactivation of Erk and Akt. Our results argue for a causal link between PKCε overexpression and prostate cancer development.
Authors:
Fernando Benavides; Jorge Blando; Carlos J Perez; Rachana Garg; Claudio J Conti; John DiGiovanni; Marcelo G Kazanietz
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-01-15
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  10     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-21     Completed Date:  2011-04-28     Revised Date:  2012-01-16    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  268-77     Citation Subset:  IM    
Affiliation:
Department of Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA.
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MeSH Terms
Descriptor/Qualifier:
Androgen-Binding Protein / genetics
Animals
Apoptosis
Cell Line, Tumor
Male
Mice
Mice, Transgenic
Phosphorylation
Precancerous Conditions / enzymology*,  pathology
Promoter Regions, Genetic
Prostate / enzymology,  pathology
Prostatic Hyperplasia / pathology
Prostatic Intraepithelial Neoplasia / enzymology*,  pathology
Prostatic Neoplasms / enzymology*,  pathology
Protein Kinase C-alpha / metabolism
Protein Kinase C-delta / metabolism
Protein Kinase C-epsilon / genetics,  metabolism*
Proto-Oncogene Proteins c-akt / metabolism
Rats
Ribosomal Protein S6 Kinases / metabolism
STAT3 Transcription Factor / metabolism
Grant Support
ID/Acronym/Agency:
P30 CA16672-30/CA/NCI NIH HHS; R01 CA089202-10/CA/NCI NIH HHS; R01-CA89202/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Androgen-Binding Protein; 0/STAT3 Transcription Factor; 0/probasin; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.1/Ribosomal Protein S6 Kinases; EC 2.7.11.13/Protein Kinase C-alpha; EC 2.7.11.13/Protein Kinase C-delta; EC 2.7.11.13/Protein Kinase C-epsilon
Comments/Corrections
Comment In:
Cell Cycle. 2011 Feb 1;10(3):379   [PMID:  21270526 ]
Cell Cycle. 2011 Feb 1;10(3):378   [PMID:  21270525 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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