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. Author manuscript; available in PMC: 2015 Mar 28.
Published in final edited form as: Life Sci. 2014 Feb 2;100(1):25–34. doi: 10.1016/j.lfs.2014.01.072

Fig. 4.

Fig. 4

Inhibition of EGFR and ERK tyrosine phosphorylation by gefitinib. (A) The ability of NTS to caused EGFR tyrosine phosphorylation was investigated as a function of gefitinib concentration using NCI-H1299 cells. The P-EGFR and total EGFR is shown. (B) The mean value ± S.D. of 4 determinations is indicated; p < 0.01, ** relative to control; p < 0.05a; p < 0.01, aa relative to NTS by ANOVA. (C) ERK tyrosine phosphorylation was determined after addition of 100 nM NTS to NCI-H1299 cells in the absence or presence of 1 or 10 µg/ml gefitinib. The P-ERK and total ERK are shown. (D) The mean value ± S.D. of 3 experiments is indicated; p < 0.01 relative to control, **; p < 0.01 relative to 100 nM NTS; p < 0.05, a; p < 0.01, aa by ANOVA. (E) The increase in EGFR transactivation caused by addition of 100 nM NTS to NCI-H1299 cells was inhibited by 5 µg/ml anti-TGFα but not anti-HB-EGF or anti-amphiregulin (Amph). The P-EGFR and total EGFR are shown. (F) The mean value ± S.D. of 4 experiments is indicated; p < 0.05, *; p , 0.01, ** relative to control; p < 0.05, a; p < 0.01, aa relative to 100 nM NTS by ANOVA.