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. 2009 Sep 14;101(1):167–172. doi: 10.1111/j.1349-7006.2009.01368.x

Figure 1.

Figure 1

 Activation of Src in non‐small cell lung cancer cells with or without MET amplification. (A) HCC827 cells, their gefitinib‐resistant clones with MET amplification (HCC827 GR5 and GR6), PC9 cells, and their gefitinib‐resistant clone with a secondary T790M mutation of epidermal growth factor receptor (PC9/ZD) were incubated for 24 h in medium containing 10% serum. Cell lysates were then prepared and subjected to immunoblot analysis with antibodies to phosphorylated (p‐) or total forms of MET, ErbB3, and Src as well as with those to β‐actin (loading control). (B) H1299 and H460 cells without MET amplification, and H1838, EBC‐1, and H820 cells with MET amplification were incubated for 24 h in medium containing 10% serum. Cell lysates were then prepared and subjected to immunoblot analysis with antibodies to phosphorylated (p‐) or total forms of MET and Src as well as with those to β‐actin (loading control).