Correlations of iodide ions with vascular endothelial growth factor and its receptors during the proliferation of vascular endothelial cells.

The aim of this study was to explore the correlations of iodide ions with vascular endothelial growth factor (VEGF) and its receptors during the proliferation of vascular endothelial cells (VECs). The proliferation rates of VECs in the presence of iodide ions and VEGF inhibitor were determined using the CCK-8 method. The effect of iodide ions on the phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR-2) was observed using Western blot analysis. In the presence of 300 µg/L iodide ions, the application of VEGF inhibitor did not inhibit VEC proliferation (P < 0.05). At a certain concentration, iodide ions upregulated the phosphorylation level of VEGFR-2 at the Tyr1214 site (P < 0.05). Iodide ions did not influence the phosphorylation of VEGFR-2 at the Tyr1175 and Tyr951 sites. At an appropriate concentration, iodide ions serve as an independent VEC proliferation-promoting factor. They mediate VEC migration by stimulating the upregulation of the phosphorylation level of VEGFR-2 (Tyr1214) and do not influence VEGFR-2 phosphorylation at Tyr1175. Therefore, their VEC proliferation-promoting effect is independent of membrane receptors.

FP3: a novel VEGF blocker with antiangiogenic effects in vitro and antitumour effects in vivo.

BACKGROUND Vascular endothelial growth factor (VEGF) is a critical promoter of blood vessel growth during embryonic development and neovascularisation in tumours. VEGF serves as a logical target for antiangiogenic cancer therapy because of its fundamental role in tumour angiogenesis. This study is to investigate the inhibitory effects of FP3, a novel VEGF blocker, on angiogenesis in vitro and tumour growth in vivo. METHODS The inhibitory effects of FP3 on angiogenesis in vitro were evaluated by using human umbilical vein endothelial cells (HUVECs) and rat aortic ring. The inhibitory effects of FP3 on tumour growth and angiogenesis in vivo were evaluated in a human non-small-cell lung cancer (NSCLC) cell line A549 tumour xenograft model with the methods of tumour growth regression assay and immunohistochemical staining, respectively. RESULTS In experiments with HUVECs, FP3 inhibited cell proliferation and migration. In rat aortic ring assay, FP3 suppressed VEGF-induced vessel sprouting. In tumour growth regression assay, FP3 significantly blocked the growth of A549 tumour in the subcutaneous tumour xenograft model and dramatically decreased the vessel density of tumour. CONCLUSIONS FP3 has excellent inhibitory effects on tumour angiogenesis both in vitro and in vivo, therefore it could be used as an effective antiangiogenic agent.