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. 2013 Jul 12;13:69. doi: 10.1186/1475-2867-13-69

Figure 3.

Figure 3

Effect of AL on STAT3 Pathway in both HUVECs and SW620 cancer cells. A(A1), AL suppressed the activation of VEGFR2 triggered by VEGF in endothelial cell. (A2), inhibition pospho-VEGFR2 resulted in a diminished activation of STAT3 in endothelial cells in dose dependent manner. HUVECs were first starved in serum-free ECM for 7–9 h and then pretreated with AL at various concentrations for periods with or without VEGF(50 ng/mL) for 5 ~ 20 min. Total VEGFR2 and STAT3 verified equal protein loading by Western blotting, as described in “Material and Methods.” B(B1), AL suppressed phospho-STAT3 levels in SW620 cell line in a dose manner. Tumor cells were directly treated with the indicated concentration of AL for different duration. The same blots were stripped and reprobed with STAT3 antibody to verify equal protein loading. (B2), AL(200 μmmol/L) suppresses STAT3-regulated genes products (Bcl-xL c-Myc and VEGF) in SW620 cells in time-dependently. β-actin was used as an corresponding internal control to show equal protein loading.