Figure 3
From: Activation of HER family members in gastric carcinoma cells mediates resistance to MET inhibition
Activation of AKT and MAPK pathways is required for resistance to MET blocking. A) WB analysis of total GTL16 lysates. PHA treatment or MET silencing (DOXY) resulted in strong impairment of MET, EGFR, HER3, AKT and p42/44 MAPK phosphorylation. In these conditions, stimulation with EGF (5 ng/ml) or HRG1-β1 (10 ng/ml) restored AKT and MAPK activation. B) Cell viability assay in PHA-inhibited or not GTL16 cells. The presence of AKT and MAPK inhibitors abrogated the resistance to MET inactivation obtained with the two ligands (*** P < 0,001), while each inhibitor alone has only a partial effect.. C) WB analysis to control the effectiveness of LY294002 and U0126.