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目的探讨选择性环氧化酶-2(COX-2)抑制剂塞来昔布对乳腺癌SKBR-3细胞生长的影响及机制。方法用不同浓度的塞来昔布处理SKBR-3细胞后,采用CCK-8法检测塞来昔布对SKBR-3细胞增殖活性的影响;流式细胞仪检测细胞周期;酶联免疫吸附试验(ELISA)检测前列腺素E2(PGE2)的释放水平;Western Blot法测定各浓度塞来昔布刺激SKBR-3细胞后Caspase-3被酶解激活情况。结果塞来昔布对SKBR-3细胞的增殖抑制作用呈剂量-时间依赖性;随着塞来昔布浓度的增加,G0/G1期细胞阻滞,S期细胞比例明显减少;塞来昔布明显减少PGE2的释放水平;Caspase-3在细胞凋亡早期被激活,在凋亡晚期则无表达。结论塞来昔布能有效抑制乳腺癌SKBR-3细胞的增殖,诱导其凋亡;其作用机制可能与COX-2表达下调、抑制PGE2水平和促进Caspase-3的活化有关。
Objective To investigate the effect of selective cyclooxygenase-2 (COX-2) inhibitor celecoxib on the growth of breast cancer SKBR-3 cells and its mechanism. Methods The SKBR-3 cells were treated with different concentrations of celecoxib. The effects of celecoxib on the proliferation of SKBR-3 cells were detected by CCK-8 assay. The cell cycle was detected by flow cytometry. ELISA was used to detect the release of prostaglandin E2 (PGE2). The activity of Caspase-3 was determined by Western Blot after the celecoxib stimulated SKBR-3 cells. Results Celecoxib inhibited the proliferation of SKBR-3 cells in a time-and dose-dependent manner. With the increase of celecoxib concentration, the cells in G0 / G1 phase were arrested and the percentage of cells in S phase was significantly decreased. Celecoxib Significantly reduced the release of PGE2; Caspase-3 was activated in the early stage of apoptosis, but no expression in late stage of apoptosis. Conclusion Celecoxib can effectively inhibit the proliferation and induce the apoptosis of breast cancer SKBR-3 cells. The mechanism may be related to the down-regulation of COX-2, the inhibition of PGE2 and the activation of Caspase-3.