Epoxyquinol B shows antiangiogenic and antitumor effects by inhibiting VEGFR2, EGFR, FGFR, and PDGFR.

摘要: Angiogenesis is the development of new blood vessels to provide oxygen and nutrients indispensable for solid tumor growth. Therefore, inhibition angiogenesis an important modality cancer chemotherapy. Here we report antiangiogenic mechanism antitumor effects epoxyquinol B (EPQB), which was isolated from fungal metabolites. Short-term treatment EPQB resulted in reduction growth number directed a murine xenografts model. Furthermore, inhibited vascular endothelial factor (VEGF)-induced migration tube formation human umbilical vein cells (HUVECs) without cytotoxicity. VEGF-stimulated phosphorylation VEGF receptor 2 (VEGFR2), phospholipase Cgamma-1 (PLCgamma1), p44/42 MAP kinases (ERK) by dose-dependent manner, vitro assay using kinase domain VEGFR2 showed that covalently bound kinase. Its binding site on different SU5614, well-known inhibitor. Interestingly, factor-induced activation not only but also epidermal (EGFR), fibroblast (FGFR), platelet-derived (PDGFR), suggesting novel multiple These findings suggest would be good lead compound potent drugs.