| Transgenic overexpression of PKCε in the mouse prostate induces preneoplastic lesions. | |
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MedLine Citation:
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PMID: 21224724 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Fernando Benavides; Jorge Blando; Carlos J Perez; Rachana Garg; Claudio J Conti; John DiGiovanni; Marcelo G Kazanietz |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2011-01-15 |
Journal Detail:
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Title: Cell cycle (Georgetown, Tex.) Volume: 10 ISSN: 1551-4005 ISO Abbreviation: Cell Cycle Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2011-01-21 Completed Date: 2011-04-28 Revised Date: 2012-01-16 |
Medline Journal Info:
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Nlm Unique ID: 101137841 Medline TA: Cell Cycle Country: United States |
Other Details:
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Languages: eng Pagination: 268-77 Citation Subset: IM |
Affiliation:
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Department of Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Androgen-Binding Protein
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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:
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P30 CA16672-30/CA/NCI NIH HHS; R01 CA089202-10/CA/NCI NIH HHS; R01-CA89202/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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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:
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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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