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. 2019 Jun 13;11(6):823. doi: 10.3390/cancers11060823

Figure 4.

Figure 4

CompC reduced cell viability, tube formation, cell migration, and vascular endothelial growth factors (VEGF)-induced signal transduction in human umbilical vein endothelial cells (HUVECs). (A) HUVECs were treated with CompC (1–20 μM), an MTT assay was performed, and the percentage of cell viability is plotted in (A). (B) The HUVEC suspension was added to Matrigel-coated wells on a 24-well plate. CompC (1–10 μM) was added to endothelial growth media kit 2 (EGM-2) and incubated for 18 h. The cells were stained with Diff-Quik and photographed (40×). (C–E) HUVECs were grown to 70–80% confluence in a 6-cm culture dish in EGM-2 medium, and some areas were denuded. Cells were then incubated in the culture medium containing various concentrations of CompC and photographed in (C) (100×). The number of HUVECs that migrated to the acellular area was counted and plotted in (D) (time-dependency) and (E) (dose-dependency). (F) HUVECs were serum-starved by incubation with endothelial cell basal medium (EBM) for 24 h. Cells were treated with EBM containing 50 ng/mL human VEGF (hVEGF) for the indicated times in the presence of vehicle (−) or 10 μM CompC (+). Cell lysates were analyzed by western blotting with antibodies against total and phosphorylated hVEGF receptor (hVEGFR) and other signaling proteins. * p < 0.05, ** p < 0.01, and *** p < 0.001, compared with vehicle-treated control cells.