Vascular endothelial growth factor receptor-3 promotes breast cancer cell proliferation, motility and survival in vitro and tumor formation in vivo

• Published in: Cell cycle (Georgetown, Tex.) Vol. 8; no. 14; pp. 2266 - 2280
• Main Authors: Kurenova, Elena V., Hunt, Darrell L., He, Dihua, Fu, Ann D., Massoll, Nicole A., Golubovskaya, Vita M., Garces, Christopher A., Cance, William G.
• Format: Journal Article
• Language: English
• Published: United States Taylor & Francis 15-07-2009
• Subjects: Animals; Binding; Biology; Bioscience; Breast Neoplasms - enzymology; Breast Neoplasms - pathology; Calcium; Cancer; Cell; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cell Survival; Cycle; Enzyme Inhibitors - pharmacology; Estrogens - pharmacology; Female; Gene Expression Regulation, Neoplastic; Humans; Landes; Mice; Mice, Nude; Organogenesis; Proteins; RNA Interference; RNA, Small Interfering - metabolism; Staurosporine - pharmacology; Transplantation, Heterologous; Vascular Endothelial Growth Factor Receptor-3 - genetics; Vascular Endothelial Growth Factor Receptor-3 - metabolism
• ISSN: 1538-4101; 1551-4005
• DOI: 10.4161/cc.8.14.9101

Vascular endothelial growth factor receptor-3 is a receptor tyrosine kinase that is overexpressed in some human carcinomas, but its role in tumorigenesis has not been fully elucidated. We examined VEGFR-3 expression in normal, nonneoplastic and early stage malignant breast tissues and have shown that VEGFR-3 upregulation in breast cancer preceded tumor cell invasion, suggesting that VEGFR-3 may function as a survival signal. We characterized the biological effects of VEGFR-3 overexpression in human breast cancer cells based on two approaches: Gain of function by overexpressing VEGFR-3 in MCF-7 breast cancer cells and loss of function by RNAi-mediated silencing of VEGFR-3 in MCF-7-VEGFR-3 and BT474 cells.