1. Antitumor effects of synthetic VEGF-receptor binding antagonist, VGA1155.
- Author
-
Ueda Y, Yamagishi T, Samata K, Hirayama N, Aozuka Y, Tanaka M, Nakaike S, and Saiki I
- Subjects
- Animals, Antineoplastic Agents pharmacology, Breast Neoplasms blood supply, Breast Neoplasms drug therapy, Breast Neoplasms pathology, Carcinoma, Non-Small-Cell Lung blood supply, Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung pathology, Carcinoma, Squamous Cell blood supply, Carcinoma, Squamous Cell drug therapy, Carcinoma, Squamous Cell pathology, Cell Growth Processes drug effects, Colonic Neoplasms blood supply, Colonic Neoplasms drug therapy, Colonic Neoplasms pathology, Humans, Lung Neoplasms blood supply, Lung Neoplasms drug therapy, Lung Neoplasms pathology, Melanoma, Experimental blood supply, Melanoma, Experimental drug therapy, Melanoma, Experimental pathology, Mice, Mice, Inbred BALB C, Mice, Nude, Neovascularization, Pathologic drug therapy, Receptors, Vascular Endothelial Growth Factor metabolism, Vascular Endothelial Growth Factor A metabolism, Xenograft Model Antitumor Assays, Benzoates pharmacology, Receptors, Vascular Endothelial Growth Factor antagonists & inhibitors, Vascular Endothelial Growth Factor A antagonists & inhibitors
- Abstract
Vascular endothelial growth factor (VEGF) plays key roles in tumor angiogenesis. Therefore, VEGF and its receptors are considered to be primary targets for antiangiogenic strategy during cancer chemotherapy. Our previous study reported that VGA1155, a low-molecular-weight inhibitor of the binding of VEGF, inhibited VEGF binding to KDR/Flk-1 receptor-overexpressing cells. In the present study, the antitumor effects and antimetastatic effect of VGA1155 were examined in vivo. VGA1155 suppressed the growth of human lung, breast, colon and epidermoid cancers (LC-6, HT29, MX-1, Col-1 and A431) in the nude mouse xenograft model, and pulmonary metastasis of melanoma in the spontaneous metastasis model. These results suggest that VGA1155 has antitumor effects in vivo through the inhibition of VEGF binding to its receptors.
- Published
- 2005