| First Author | Benavides F | Year | 2011 |
| Journal | Cell Cycle | Volume | 10 |
| Issue | 2 | Pages | 268-77 |
| PubMed ID | 21224724 | Mgi Jnum | J:254978 |
| Mgi Id | MGI:6113776 | Doi | 10.4161/cc.10.2.14469 |
| Citation | Benavides F, et al. (2011) Transgenic overexpression of PKCepsilon in the mouse prostate induces preneoplastic lesions. Cell Cycle 10(2):268-77 |
| abstractText | It is well established that protein kinase C (PKC) isozymes play distinctive roles in mitogenic and survival signaling as well as in cancer progression. PKCepsilon, 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 PKCalpha, PKCdelta, or PKCepsilon in the prostate epithelium under the control of the rat probasin (PB) promoter. Whereas PB-PKCepsilon and PB-PKCdelta mice did not show any evident phenotype, PB-PKCepsilon 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. PKCepsilon overexpression was insufficient to drive neoplastic changes in the mouse prostate. Notably, overexpression of PKCepsilon 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 PKCepsilon overexpression and prostate cancer development. |
