Fig. 5
HGF/c-MET axis upregulates ETV1 via ERK1/2 activation. (A) The expression of ETV1 in PLC/PRF/5 cells treated with different concentrations of recombinant HGF. (B) The expression of ETV1 in HepG2 cells treated with different concentrations of HGF. (C) Relative luciferase activities of ETV1 promoter reporter vectors in indicated cells upon treatment with HGF. (D) Western blotting assays of ETV1, Akt, p-Akt, ERK1/2, p-ERK1/2, JNK, p-JNK, p38, p-p38, proceed with PI3K inhibitor (LY294002), ERK1/2 inhibitor (SCH772984), JNK inhibitor (SP600125), and p38 inhibitor (SB203580) upon HGF treatment in PLC/PRF/5 cells. (E) Relative luciferase reporter assays of PLC/PRF/5 cells transfected with serially truncated or mutant ETV1 promoter luciferase constructs treated with or without HGF. (F-H) The relative promoter luciferase activity, mRNA, and protein levels of ETV1 in the PLC/PRF/5 cells after transfection with shELK1 or control shRNA in the presence of HGF. (I) ChIP assays verified the direct binding of ELK1 to the ETV1 promoter in HCC cells. * Represented p < 0.05. All data were displayed as Mean ± SD