Fig. 6From: HCC-derived EGFR mutants are functioning, EGF-dependent, and erlotinib-resistantErlotinib induces differential degree of inhibition of EGFR, Akt, and Erk phosphorylation among cells harboring different EGFRs. NIH-3T3 cells harboring EGFR WT and mutants were cultured in DMEM containing 4% FBS with different concentrations of erlotinib (0, 0.3, and 5 µM). Immunoblotting shows the effect of erlotinib on EGFR tyrosine phosphorylation after 24 h treatment (a), the effect of erlotinib on AKT and ERK phosphorylation after 24 h treatment, β-actin used as a loading control (b). Graphic presentations of relative band intensities of AKT and ERK phosphorylation in cells treated with erlotinib, presented as mean ± SEM in c, and d respectivelyBack to article page