PKC Epsilon: A Novel Oncogenic Player in Prostate Cancer

Abstract

Protein kinase C epsilon (PKCe), a member of the PKC family of phorbol ester/diacylglycerol receptors, is up-regulated in many human cancers, including prostate cancer. We recently demonstrated that PKCe is an essential mediator of NF-kB activation in prostate cancer (Garg et al., JBC, 287, 37570 37582, 2012). In this research, we wish to determine if PKCe regulates TNFa-signaling to mediate its effect on NF-kB activation. Using a specific PKCe antagonist, we demonstrated that PKCe plays essential role in the TNFa-induced phosphorylation of TNF receptor in prostate cancer cells. We have previously identified that PKCe regulates NF-kB responsive genes in prostate cancer cells, including cyclooxygenase-2 (COX-2) (JBC, 2012). COX-2 has been reported to be up-regulated in metastatic prostate cancer. As PKCe plays an important role in prostate cancer cell survival and cooperates with other oncogenic insults, herein we aim to determine if PKCe regulates COX-2 activation during prostate tumorigenesis. In the previous funding period we have demonstrated that COX- 2 is overexpressed in human prostate cancer cell lines similar to PKCe and NF-kB. It was found that PKCe regulates COX-2 activation and PGE2 levels in prostate cancer as well as normal human prostate epithelial cells. In the present report, we present our continued efforts on the in-depth determination of the role of PKCe in COX-2 activation in prostate cancer and also to investigate if COX-2 mediates PKCe responses in prostate cancer. Our results showed that transgenic overexpression of PKCe in the mouse prostate causes preneoplastic lesions with elevated COX-2 levels. Interestingly, when we intercrossed the prostate-specific PKCe transgenic mice with mice haploinsufficient for Pten, a common genetic alteration in human prostate cancer, the resulting compound mutant mice (PB-PKCe;Pten+/- mice) developed fully invasive adenocarcinoma with NF-kB hyperactivation and high COX-2 levels. Likewise, stable overexpression

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Document Details

Document Type
Technical Report
Publication Date
Sep 01, 2014
Accession Number
ADA612051

Entities

People

  • Rachana Garg

Organizations

  • University of Pennsylvania

Tags

DTIC Thesaurus Topics

  • Adenocarcinoma
  • Biomedical Research
  • Cancer
  • Carcinoma
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Department Of Defense
  • Diseases And Disorders
  • Epithelial Cells
  • Inhibition
  • Inhibitors
  • Kinases
  • Neoplasms
  • Prostate Cancer
  • Regulations
  • Survival

Fields of Study

  • Biology

Readers

  • Canadian European Scientific Immigration and Epilepsy Clearance Studies
  • Cellular and Molecular Pathways of Apoptosis.
  • Molecular and genetic basis of cancer.

Technology Areas

  • Biotechnology
  • Biotechnology - Cancer Biotech