Role of Caveolin-1 in Prostate Cancer Angiogenesis
Abstract
We have made a significant progress toward our stated goals. Notable achievements for the past year of funding include comprehensive documentation that prostate cancer cell derived, secreted caveolin-1 is taken up by cancer cells and tumor associated endothelial cells (Tahir et al, Cancer Res 2008). This autocrine/paracrine activity of secreted caveolin-1 promotes malignant progression by stimulation of specific angiogenic activities. We have shown in cav-1 negative LP-LNCaP cells that adenoviral vector mediated expression of cav-1 stimulated VEGF mediated VEGFR2 autophosphorylation and activated downstream signaling. We are further exploring cav-1 mediated angiogenic signaling in endothelial cell models, including the possibility of direct interactions between cav-1 and VEGFR2. Our animal model studies have shown that systemic delivery of cav-1 antiserum suppresses primary tumor growth and lung metastasis in a pre-established metastasis prostate cancer model. Moreover, systemic treatment with cav-1 Ab increased survival in the mouse model of prostate cancer (see Fig 6-8). Our results indicate that cav-1 may be a clinically useful biomarker of prostate cancer progression and a potential therapeutic target.
Document Details
- Document Type
- Technical Report
- Publication Date
- Dec 01, 2008
- Accession Number
- ADA495845
Entities
People
- Timothy C Thompson
Organizations
- The University of Texas MD Anderson Cancer Center