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. 2019 Sep 9;110(11):3584–3594. doi: 10.1111/cas.14180

Figure 2.

Figure 2

Both the c‐mesenchymal‐epithelial transition factor (c‐Met) inhibitor crizotinib and the c‐Met‐targeting monoclonal antibody (c‐Met mAb) inhibit phosphorylation of the c‐Met downstream targets, AKT and ERK1/2, only in resistant HCC827 cells with elevated phospho‐c‐Met levels. A, Parental and AZD9291‐resistant HCC827 cells were lysed and immunoblotted with anti‐c‐Met and anti‐phospho‐c‐Met antibodies. Relative protein levels of c‐Met and phospho‐c‐Met were normalized to endogenous GAPDH protein for each sample. Data are expressed as mean ± SD of three individual experiments. *P < .05, **P < .01 vs parental HCC827 cells. B, HCC827, HA1, and HG1 cells were treated with AZD9291 plus 100 nmol/L crizotinib or 1 μg/mL c‐Met mAb for 6 h. Whole‐cell lysates were analyzed by western blotting using the indicated antibodies