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目的探讨环氧合酶-2(COX-2)抑制剂SC236对肾癌细胞RCC-949生物学行为的影响。方法体外培养RCC-949细胞,不同浓度的SC236与之作用24、487、2 h,四甲基偶氮唑盐(MTT)法检测细胞的生长状况;50、150μmol/L SC236作用RCC-949细胞48 h,RT-PCR法检测COX-2 mRNA的表达;50、100μmol/L SC236作用RCC-949细胞24 h,ELISA法检测SC236细胞上清前列腺素(PGE2)的生成情况;100μmol/L SC236作用RCC-949细胞24 h后流式细胞仪检测细胞周期与凋亡情况。结果 SC236呈时间-剂量依赖性抑制RCC-949细胞的增殖;RT-PCR结果显示SC236能降低RCC-949细胞COX-2 mRNA的表达;不同浓度的SC236均能下调PEG2的释放,与对照组比较差异有统计学意义(P<0.05);流式细胞术结果表明不同浓度的SC236均能诱导RCC-949细胞发生凋亡,凋亡率同对照组比较差异有统计学意义(P<0.05)。结论特异性COX-2抑制剂SC236能通过COX-2依赖途径抑制肾癌细胞RCC-949增殖,能下调PEG2的释放,诱导了其发生凋亡。
Objective To investigate the effect of cyclooxygenase-2 (COX-2) inhibitor SC236 on the biological behavior of renal cell carcinoma cell line RCC-949. Methods RCC-949 cells were cultured in vitro. SC236 cells were treated with different concentrations of SC236 for 24,487,2 h. The growth of RCC-949 cells was detected by methyl thiazolyl tetrazolium (MTT) assay. The expression of COX-2 mRNA was detected by RT-PCR. The proliferation of SCC-949 cells was induced by 50,100μmol / L SC236 for 24 hours. The production of prostaglandin (PGE2) in SC236 cells was detected by ELISA. The effect of 100μmol / Cell cycle and apoptosis were detected by flow cytometry after 24 hours in RCC-949 cells. Results SC236 inhibited the proliferation of RCC-949 cells in a time-and dose-dependent manner. The results of RT-PCR showed that SC236 could reduce the expression of COX-2 mRNA in RCC-949 cells. SC236 all decreased the release of PEG2 compared with the control group The difference was statistically significant (P <0.05). The results of flow cytometry showed that different concentrations of SC236 could induce apoptosis of RCC-949 cells. The apoptosis rate was significantly different from that of the control group (P <0.05). CONCLUSIONS: The specific COX-2 inhibitor SC236 can inhibit the proliferation of RCC-949 cells by down-regulating the release of PEG2 and inducing its apoptosis through COX-2-dependent pathway.