Skip to main content
. 2016 Feb 22;7(14):18229–18246. doi: 10.18632/oncotarget.7571

Figure 4. L-FABP increases cell migration activity via VEGFR2/Src signaling and the FAK/cdc42 pathway.

Figure 4

A. Phosphorylation of VEGFR2 in Hus/L-FABP and Hus/Vector (vector-only control) cells assessed by immunoprecipitation (IP) with a VEGFR2 antibody and blotting with a phospho-tyrosine antibody. *p < 0.05 versus Hus/Vector control. B. Phosphorylation of Src (Tyr416) and FAK (Tyr397) in Hus/L-FABP and Hus/Vector cells analyzed by western blotting. **p < 0.01 versus Hus/Vector control. C. Small GTPase binding in Hus/L-FABP or Hus/Vector cells. Active cdc42 and Rac1, but not RhoA, were detected by western blotting analysis. ***p < 0.001 for cdc42 activity versus Hus/Vector control. D. Wound-healing migration (2D migration activity) of Hus/L-FABP and Hus/Vector cells over 24 h. ***p < 0.001 versus Hus/Vector control. E. Migration activity of Hus/L-FABP and Hus/Vector cells seeded onto Boyden chambers and allowed to migrate toward 10% serum-containing medium for 16 h. ***p < 0.001 versus Hus/Vector control. F. Migration activity of Hus/L-FABP cells treated with PP1 (Src inhibitor: 5 or 10 μM) or Sorafenib (VEGFR2 inhibitor: 1, 2, or 4 μM) for 16 h. ***p < 0.001 versus DMSO-treated control group.

HHS Vulnerability Disclosure