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目的:探讨环氧化酶-2抑制剂JTE-522是否对人子宫内膜癌细胞株RL95-2细胞有抑制增殖和诱导凋亡的作用及其分子机理.方法:应用体外噻唑兰法、琼脂糖凝胶电泳、酶联免疫试验、流式细胞术、RT-PCR及Western blot等方法研究JTE-522对RL952细胞增殖和凋亡的作用及其分子机理.结果:JTE522抑制RL95-2细胞的增殖、诱导其凋亡、引起G_0/G_1期阻滞和 S期抑制,并伴有COX-2 mRNA、磷酸化 Rb、CDK4蛋白表达的抑制及 p53,p21和cyclin D_1蛋白表达水平的上调.另外,细胞经 JTE-522处理后,还可见caspase-3活性的增加.结论:JTE-522抑制RL95-2细胞的增殖及诱导其凋亡,可能与COX-2mRNA,磷酸化Rb、CDK4蛋白水平的下降及 p53,p21和 cyclin D_1蛋白表达的上调有关,还可能与caspase-3的激活有关.
Objective: To investigate whether cyclooxygenase-2 inhibitor JTE-522 inhibits proliferation and induces apoptosis in human endometrial carcinoma cell line RL95-2 and its molecular mechanism.Methods: Thiazide blue method, agar The effect of JTE-522 on the proliferation and apoptosis of RL952 cells and its molecular mechanism were studied by using gel electrophoresis, enzyme-linked immunosorbent assay, flow cytometry, RT-PCR and Western blot.Results: The inhibitory effect of JTE522 on RL95-2 cells Proliferation and induction of apoptosis, G0 / G1 phase arrest and S phase inhibition, accompanied by the inhibition of COX-2 mRNA, phosphorylation of Rb, CDK4 protein expression and p53, p21 and cyclinD1 protein levels. , And the increase of caspase-3 activity after treated with JTE-522.Conclusion: JTE-522 inhibits the proliferation and induces the apoptosis of RL95-2 cells, which may be related to the expression of COX-2mRNA, phosphorylated Rb and CDK4 Decreased and p53, p21 and cyclinD1 protein expression upregulation, may also be related to the activation of caspase-3.