Cooperativity Between Oncogenic PKC Epsilon and Pten Loss in Prostate Cancer Progression
Technical Report,30 Sep 2015,29 Sep 2016
Trustees of the University of Pennsylvania Philadelphia United States
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The main objective of our studies is to elucidate the mechanisms by which PKC, in conjunction with Pten loss, lead to malignant transformation and metastasis, through an autocrine mechanism that involves the release of the chemokine CXCL13. During the first year we acquired new evidence that CXCL13 levels are elevated in prostate cancer cells and that PKC is causally associated with the elevated production and release of this chemokine. We also initiated studies to dissect the signaling mechanisms that mediate CXCL13 induction. We took advantage of a cellular model that we generated in our laboratory in which PKC was overexpressed using a lentivirus in a Pten-deficient background. We also remediated the issue of loss of stable PKC expression in prostate epithelial cell lines by generating a new PKC lentivirus. Our research may impact on our understanding of the molecular mechanisms of prostate tumorigenesis, and may have significant prognostic and therapeutic implications.
- Medicine and Medical Research