Inhibition of Stromal PlGF Suppresses the Growth of Prostate Cancer XenograftsReport as inadecuate




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1

Laboratory for Molecular Cellular Biology, Center for Anatomy and Cell Biology, Medical University of Vienna, Vienna 1090, Austria

2

Department of Immunology, Institute for Cancer Research, The Norwegian Radium Hospital, Montebello, Oslo N-0310, Norway





*

Author to whom correspondence should be addressed.



Abstract The growth and vascularization of prostate cancer is dependent on interactions between cancer cells and supporting stromal cells. The primary stromal cell type found in prostate tumors is the carcinoma-associated fibroblast, which produces placental growth factor PlGF. PlGF is a member of the vascular endothelial growth factor VEGF family of angiogenic molecules and PlGF mRNA levels increase after androgen deprivation therapy in prostate cancer. In this study, we show that PlGF has a direct dose-dependent proliferative effect on human PC-3 prostate cancer cells in vitro and fibroblast-derived PlGF increases PC-3 proliferation in co-culture. In xenograft tumor models, intratumoral administration of murine PlGF siRNA reduced stromal-derived PlGF expression, reduced tumor burden and decreased the number of Ki-67 positive proliferating cells associated with reduced vascular density. These data show that targeting stromal PlGF expression may represent a therapeutic target for the treatment of prostate cancer. View Full-Text

Keywords: prostate cancer; placental growth factor; xenograft model; tumor-host interaction; tumor angiogenesis prostate cancer; placental growth factor; xenograft model; tumor-host interaction; tumor angiogenesis





Author: Karin Zins 1, Anita Thomas 1, Trevor Lucas 1, Mouldy Sioud 2, Seyedhossein Aharinejad 1 and Dietmar Abraham 1,*

Source: http://mdpi.com/



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