Figure 3.

Distinct responses mediated by WT and V370D mutant MET. A, Expression and tyrosine phosphorylation of MET receptor in PC‐9 MET receptor‐knockout (PC‐9 METKO) cells. Cells were stimulated with HGF for 10 min. MET, p‐MET, p‐AKT, and GAPDH were detected by western blotting. B, Expression and activation of MET‐WT and MET‐V370D and response to HGF stimulation. Cells were stimulated with HGF for 10 min. MET, p‐MET, p‐AKT, and GAPDH were detected by western blotting. C, Cell viability after treatment with gefitinib and hepatocyte growth factor (HGF) in PC‐9 WT and PC‐9 V370D cells. Cells were treated with or without gefitinib or HGF for 3 d. Data represent mean ± SE (n = 3). *P < .05. D, Effect of MET kinase inhibitor on viability of CHO‐WT and CHO‐V370D cells. Cells were cultured in the absence or presence of PHA665752 in medium supplemented with different FBS concentrations for 24 or 48 h. Data represent mean ± SD (n = 4). E, Change in phosphorylation of RTK in CHO‐WT cells and CHO‐V370D cells (#1‐#3, independent clones) cultured under survival/growth‐stressed conditions. The cells were cultured in medium supplemented with 0.01% FBS and 20 ng/mL HGF for 10 d