Abstract
c-Met amplification is one of the reasons for Gefitinib resistance in NSCLC patients. 1.Explore the mechanism of the up-regulation of c-Met by Cox-2; 2.Combination of Cox-2 inhibitor and Gefitinib can overcome Gefitinib resistance in cells or animal study; 3.Test the expression pattern or activity of Cox-2 in NSCLC patients, and evaluate the possibility of Cox-2 serving as biomarker for Gefitinib resistance and prognosis for NSCLC patients. 1.Both c-met and Cox-2 are highly expressed in Gefitinib resistant lung cancer cell lines; 2.Cox-2 is highly expressed in malignant lung adenocarcinoma than in matched normal tissues; 3.Inhibition of Cox-2 can decrease c-Met expression， and promote apoptosis induced by Gefitinib in Gefitinib resistant cells. Up-regulation of c-Met by Cox-2 promotes resistance of Gefitinib in NSCLC patients
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