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Prostate. 2011 Jun 15;71(9):946-54. doi: 10.1002/pros.21310. Epub 2010 Nov 23.

PKCδ activation mediates angiogenesis via NADPH oxidase activity in PC-3 prostate cancer cells.

Author information

1
Department of Chemical and Systems Biology, Stanford University, School of Medicine, Stanford, California 94305-5174, USA.

Abstract

BACKGROUND:

PKCδ is generally known as a pro-apoptotic and anti-proliferative enzyme in human prostate cancer cells.

METHODS:

Here, we investigated the role of PKCδ on the growth of PC-3 human prostate cancer cells in vivo and in vitro.

RESULTS:

We found that sustained treatment with a specific PKCδ activator (ψδ receptor for active C kinase, ψδRACK) increased growth of PC-3 xenografts. There was increased levels of HIF-1α, vascular endothelial growth factor and CD31-positive cells in PC-3 xenografts, representative of increased tumor angiogenesis. Mechanistically, PKCδ activation increased the levels of reactive oxygen species (ROS) by binding to and phosphorylating NADPH oxidase, which induced its activity. Also, PKCδ-induced activation of NADPH oxidase increased the level of HIF-1α.

CONCLUSIONS:

Our results using tumors from the PC-3 xenograft model suggest that PKCδ activation increases angiogenic activity in androgen-independent PC-3 prostate cancer cells by increasing NADPH oxidase activity and HIF-1α levels and thus may partly be responsible for increased angiogenesis in advanced prostate cancer.

PMID:
21541971
PMCID:
PMC3544470
DOI:
10.1002/pros.21310
[Indexed for MEDLINE]
Free PMC Article
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