Fig. 5

rMSA activated SRC and reduced the interaction of CAV1 between EGFR to increase EGFR activation. A Western blot showing the protein and phosphorylation levels of IGF-1R/IR and AKT in the AML12 hepatocytes treated with vehicle or rMSA (75, 600 μM), with or without insulin (1, 10 nM) for 5 min. B Western blot showing the protein and phosphorylation levels of IGF-1R/IR in the AML12 hepatocytes treated with vehicle or rMSA (600 μM), with or without insulin (10 nM) at different time points. C Western blot showing the protein and phosphorylation levels of SRC in the AML12 hepatocytes treated with rMSA (600 μM) at different time points. D Western blot showing the protein and phosphorylation levels of EGFR, SRC, and AKT in the AML12 hepatocytes treated with vehicle or rMSA (600 μM) in the absence or presence of 20 μM PP1 or 2 μM Dasatinib for 2 h. E Western blot showing the protein and phosphorylation levels of EGFR in the AML12 hepatocytes treated with rMSA (600 μM) at different time points. F Western blot showing the protein and phosphorylation levels of EGFR, AKT, and FOXO1 in the AML12 hepatocytes treated with vehicle or rMSA (600 μM) in the absence or presence of 10 μM BDTX-189 or 10 μM Varlitinib for 6 h. G The AML-12 hepatocytes treated with or without rMSA (600 μM) for 2 h in the absence or presence of 2 μM Dasatinib were lysed; comparable amounts of total cell lysates immunoprecipitated with anti-CAV1 antibody were resolved by SDS/PAGE and visualized by the indicated antibodies. H Western blot showing the protein and phosphorylation levels of EGFR, AKT, and CAV1 in the AML12 hepatocytes transfected with siRNA against CAV1 (siCAV1-1 and siCAV1-2) for 48 h then treated with vehicle or rMSA (600 μM) in the absence or presence of 2 μM Dasatinib for 2 h. β-Actin was used as the internal reference (A, C, D, and F–H)