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. 2016 May 17;7(27):41067–41080. doi: 10.18632/oncotarget.9392

Figure 3. YLL545 functions via VEGFR2-dependent and independent pathways.

Figure 3

A. HUVECs were treated with different concentrations of YLL545 and vehicle control for 72 h. The expression and phosphorylation of VEGFR2, mTOR, STAT3, and ERK1/2 were measured by immunoblotting and normalized to levels of β-actin. B. Cellular thermal shift assays were conducted using HUVECs treated with 50 μM YLL545 or vehicle control. The expression of VEGFR2 was measured by immunoblotting and normalized to levels of β-actin. C. Molecular docking showed the binding mode of YLL545 with the inactive conformation of VEGFR2. D. HUVECs were treated with 5 μM YLL545 or vehicle for 24 h. The expression of ITGAV, ENG, THBS1, FN1, and TEK expression were examined by quantitative PCR. Expression levels were normalized to GAPDH expression. ***P < 0.001 vs respective control in Student's t-test.