摘要
目的观察选择性COX-2抑制剂尼美舒利对食管癌Eca-109细胞增殖、凋亡及COX-2表达的影响,并探讨与抑癌基因P27kip1的关系。方法用MTT法测定Eca-109细胞增殖;透射电镜及流式细胞仪观察细胞凋亡及细胞周期;RT-PCR法检测Eca-109细胞COX-2mRNA表达变化;Westernblot检测COX-2和P27kip1蛋白表达变化。结果尼美舒利以时间、剂量依赖方式抑制Eca-109增殖,增加G0/G1期细胞比例;呈剂量依赖性诱导细胞凋亡,降低COX-2mRNA和蛋白表达,上调P27kip1蛋白表达。结论尼美舒利可抑制食管癌Eca-109细胞增殖,使细胞周期受阻于G0/G1期并诱导细胞凋亡。其机制可能是通过下调COX-2表达和上调P27kip1蛋白表达水平实现的。
Objective To investigate the effects of selective COX-2 inhibitor nimesulide on growth inhibition, apoptosis and expression of COX-2 of human esophageal carcinoma Eca-109 cell line; and analyzed the correlation with the anti-oncogene, P27 kip1. Methods MTT assay was used to detect the proliferation of Eca-109 cell. Apoptosis and cell cycle were determined by electronic microscopy and flow cytometry. The expression of COX-2 mRNA was detected by reverse transcription polymerase chain reaction （ RT-PCR）, the protein expression of COX-2 and P27kip1 were examined by Western blot analysis. Results Nimesulide significantly inhibited the proliferation of Eca-109 cell line in a time- and dose-depenent fashion; increased the proportion of cells in the Go/G1 phase and induced apoptosis of the cells in a dose-dependent（manner）. Meanwhile, nimesulide can down-regulated the expression of COX-2 and up-regulated the expression of P27kip1 protein. Conclusion Nimesulide can inhibit the proliferation of Eca-109 cells, cause G0/G1 phase cell cycle arrest and induce apoptosis. The mechanism is probably explained with down-regulation of the expression of COX-2 and up-regulation of P27 kip1 expression.
出处
《基础医学与临床》
CSCD
北大核心
2006年第7期729-733,共5页
Basic and Clinical Medicine
基金
河北省自然科学基金(301354)
