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. Author manuscript; available in PMC: 2020 Aug 1.
Published in final edited form as: Int J Cancer. 2019 Feb 11;145(3):748–762. doi: 10.1002/ijc.32170

Figure 3.

Figure 3.

MET confers resistance predominantly through MAPK pathway activation. (a) 5-day proliferation assay testing cetuximab (12.5 μg/mL) efficacy in the SNU1076 and HSC4 HNSCC cell lines, with and without rHGF (50 ng/mL) and the MET inhibitor PHA-665752 (1 μM). Statistical significance was calculated from 3 to 5 independent experiments using one-way ANOVA test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). (b) Western blot for the indicated protein levels following 24 h treatment of cetuximab (12.5 μg/mL), with and without rHGF (50 ng/mL) and the MET inhibitor PHA-665752 (1 μM), in the SNU1076 and HSC4 HNSCC cell lines. Data represent a representative experiment (from three independent experiments) (c) 5-day proliferation assay testing cetuximab (12.5 μg/mL) efficacy in the SNU1076 and HSC4 HNSCC cell lines, with and without rHGF (50 ng/mL) and the MEK½ inhibitor PD-0325901 (25 nM). Statistical significance was calculated from three independent experiments using one-way ANOVA test (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001).