Linked Life Data

21406403

Source:http://linkedlifedata.com/resource/pubmed/id/21406403

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2011-3-16
pubmed:abstractText
Protein kinase C epsilon (PKC?), a novel PKC isoform, is overexpressed in prostate cancer (PCa) and correlates with disease aggressiveness. However, the functional contribution of PKC? to development or progression of PCa remained to be determined. Here we present the first in vivo genetic evidence that PKC? is essential for both the development and metastasis of PCa in the transgenic mouse model of prostate adenocarcinoma (TRAMP). Heterozygous or homozygous genetic deletions of PKC? in FVB/N TRAMP inhibited PCa development and metastasis as analyzed by positron emission tomography/computed tomography, tumor weight determinations, and histopathology. We also examined biomarkers associated with tumor progression in this model, including markers of survival, proliferation, angiogenesis, inflammation, and metastatic progression. To find clues about the genes regulated by PKC? and linked to the Stat3 signaling pathway, we carried out focused PCR arrays of JAK/STAT signaling in excised PCa tissues from PKC? wild-type and nullizygous TRAMP mice. Notably, PKC? loss was associated with significant downregulation of proliferative and metastatic genes C/EBP? (CCAAT/enhancer binding protein ?), CRP (C-reactive protein), CMK, EGFR (epidermal growth factor receptor), CD64, Jun B, and gp130. Taken together, our findings offer the first genetic evidence of the role of PKC? in PCa development and metastasis. PKC? may be potential target for prevention and/or treatment of PCa.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1538-7445
pubmed:author
pubmed:copyrightInfo
© 2011 AACR.
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
71
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2318-27
pubmed:meshHeading
pubmed-meshheading:21406403-Adenocarcinoma, pubmed-meshheading:21406403-Animals, pubmed-meshheading:21406403-C-Reactive Protein, pubmed-meshheading:21406403-Disease Models, Animal, pubmed-meshheading:21406403-Female, pubmed-meshheading:21406403-Gene Expression, pubmed-meshheading:21406403-Humans, pubmed-meshheading:21406403-Immunoblotting, pubmed-meshheading:21406403-Janus Kinases, pubmed-meshheading:21406403-Male, pubmed-meshheading:21406403-Mice, pubmed-meshheading:21406403-Mice, Knockout, pubmed-meshheading:21406403-Mice, Transgenic, pubmed-meshheading:21406403-Neoplasm Metastasis, pubmed-meshheading:21406403-Positron-Emission Tomography, pubmed-meshheading:21406403-Prostate, pubmed-meshheading:21406403-Prostatic Neoplasms, pubmed-meshheading:21406403-Protein Kinase C-epsilon, pubmed-meshheading:21406403-Receptor, Epidermal Growth Factor, pubmed-meshheading:21406403-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:21406403-STAT3 Transcription Factor, pubmed-meshheading:21406403-Signal Transduction, pubmed-meshheading:21406403-Tomography, X-Ray Computed
pubmed:year
2011
pubmed:articleTitle
Genetic ablation of PKC epsilon inhibits prostate cancer development and metastasis in transgenic mouse model of prostate adenocarcinoma.
pubmed:affiliation
Department of Human Oncology, Wisconsin Institute of Medical Research, Paul Carbone Comprehensive Cancer Center, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin 53792, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural