COX-2抑制剂(阿司匹林)体外抑制人食管癌细胞的生长及诱导凋亡

Objective: To investigate the biological effects of aspirin on esophageal carcinoma cells and the possible mechanism. Methods: The inhibitory effects of aspirin on proliferation of esophageal carcinoma cell lines Eca-109 and TE-13 were measured by MTT assay. Cyclooxygenase (COX)-2, Bcl-2 and Bax protein expression and apoptosis induced by aspirin of the two cell lines were detected by flow cytometry (FCM). Progesterone E2 (PGE2) in the supernatants of cell culture was measured by radioimmunoassay (RIA). Results: Aspirin inhibited the proliferations of Eca-109 and TE-13 cells in a concentration- and time dependent manner, but decreased the PGE2 level produced by the two cell lines. Aspirin treatment arrested the two cell lines at G0/G1 phase, reduced the proportion of S phase significantly (P＜0.01), and induced apparent apoptosis. Aspirin time dependently decreased the expressions of COX-2 and Bcl-2 and increased the expression of Bax of the two cell lines. Expressions of COX-2 and Bcl-2 had significant correlations with expression of Bax (P＜0.01). Conclusion: Aspirin inhibits the proliferation and inducs apoptosis of esophageal carcinoma cells. COX-2 inhibitors has the potential to be used in the chemoprevention or adjuvant treatment for esophageal carcinomas.