EGF-Induced VEGF Exerts a PI3K-Dependent Positive Feedback on ERK and AKT through VEGFR2 in Hematological In Vitro Models
Fig 5
Activation of ERK and AKT is PI3K-dependent while PLC regulates p38.
A total of 106 THP1 or Raji cells/well were cultured and pretreated for 30min with 10μM of either LY294002 or U73122 inhibitor. In order to measure p-Akt, p-ERK and p-p38, cells were then treated with EGF at 20ng/ml for 10min, 20min, 30min or 5min, 10min, 20min in THP1 or Raji cell lines, respectively. Western blot analysis showing that EGF-induced phosphorylation of ERK and AKT was inhibited in the presence of LY294002 whereas that of p38 was inhibited by U73122. Results are representatives of three independent experiments (n = 3) for each treatment condition.