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. 2015 Sep 21;10(12):2687–2696. doi: 10.1021/acschembio.5b00655

Figure 4.

Figure 4

SFK inhibition decreasing DDR2 phosphorylation and suppressing DDR2 mutated cancer cell lines. (A) DDR2 was ectopically expressed in 293T cells, and phosphorylation was measured by Western blotting with antiphosphotyrosine (4G10) after immunoprecipitation with an anti-DDR2 antibody. Cells were treated with the indicated concentration of 1 in combination with or without 1 μM of saracatinib. (B) Proliferation of NCI-H2286 and HCC-366 cells grown for 5 days in the presence of compound 1 in combination with DMSO or 1 μM of saracatinib or in the presence of different concentrations of saracatinib with DMSO. Graph shows mean ± SD from a single experiment representative of three independent experiments with three replicates per treatment per experiment. (C) DDR2 WT or SRC WT was ectopically expressed in 293T cells. Cells were treated with saracatinib. Receptor phosphorylation was measured by Western blotting with antiphosphotyrosine after immunoprecipitation with an anti-DDR2 antibody. Western blotting for anti-DDR2, anti-t-SRC, anti-p-SFK, and antiactin was performed with the same lysate. (D) DDR2 WT, DDR2 GK, SRC WT, or SRC GK was ectopically expressed in 293T cells. Cells were treated with a vehicle or dasatinib. Western blotting with antiphosphotyrosine, anti-DDR2, or total SRC was performed after immunoprecipitation with an anti-DDR2 antibody.