Toxicity of selective COX-2 inhibitor celecoxib on non-small cell lung cancer cell lines and the molecular mechanism in vitro

OBJECTIVE: To study the effect of growth inhibition and apoptosis induction in non-small cell lung cancer (NSCLC) cell lines by selective COX-2 inhibitor celecoxib and the cell molecular mechanism. METHODS: MTT assay was used to detect the growth inhibition of celecoxib on 3 NSCLC cell lines A549 (adenocarcinoma), GLC82 (adenocarcinoma), SW1573 (bronchioalveolar carcinoma). Hoechest33258 staining was used to detect cell apoptosis. Flow cytometric analysis was used to assess the cell cycle distribution and apoptosis. Western blot analysis was used to detect the expressions of COX-2, p-AKT, AKT, p-ERK and ERK proteins. RESULTS: The IC50 of celecoxib on A549, GLC82 and SW1573 were 14.7, 10.6 and 18.6 μmol/L, respectively. Celecoxib induced apoptosis in NSCLC cell lines. Apoptosis was detected after the treatment for 12 hours and stronger for 24-48 hours. Apoptosis was detected under 10-40 μmol/L concentration celecoxib treatment. P-AKT and p-ERK proteins were detected to be downregulated after the celecoxib treatment. CONCLUSION: Selective COX-2 inhibitor celecoxib can inhibit the cell signal transduction AKT and ERK pathway in NSCLC and induce apoptosis and cell growth inhibition.