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目的:探讨肿瘤坏死因子相关凋亡诱导配体(TRAIL)对肿瘤细胞中过氧化氧化还原蛋白(PRDXs)表达的影响及其机制。方法:选取肿瘤细胞,设立对照组和TRAIL处理组;用实时定量PCR法和蛋白质印迹法检测PRDXs在各种肿瘤细胞中的表达;用PCR法克隆PRDX4启动子,用萤光素酶含量测定其含量。结果:与对照组相比,TRAIL处理组中PRDX1、PRDX2、PRDX3、PRDX5和PRDX6mRNA及蛋白表达差异无统计学意义,P>0.05;PRDX4mRNA和蛋白的表达显著降低,P<0.01;放线菌素D处理8h时,TRAIL处理组与对照组中PRDX4mRNA降解近50%,差异无统计学意义,P>0.05;TRAIL显著降低pPRDX4/-979的活性呈剂量依赖方式。结论:TRAIL在转录水平上下调肿瘤细胞中PRDX4基因的表达,对PRDX4mRNA的稳定性没有影响。
Objective: To investigate the effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) on the expression of peroxiredoxin (PRDXs) in tumor cells and its mechanism. Methods: Tumor cells were selected to establish the control group and the TRAIL-treated group. The expression of PRDXs in various tumor cells was detected by real-time quantitative PCR and Western blotting. PRDX4 promoter was cloned by PCR and its luciferase content was measured content. Results: Compared with the control group, the mRNA and protein expressions of PRDX1, PRDX2, PRDX3, PRDX5 and PRDX6 in TRAIL-treated group were not significantly different (P> 0.05); the expression of PRDX4 mRNA and protein was significantly decreased D treatment 8h, TRAIL treatment group and control group PRDX4 mRNA degradation nearly 50%, the difference was not statistically significant, P> 0.05; TRAIL significantly reduce the activity of pPRDX4 / -979 in a dose-dependent manner. Conclusion: TRAIL downregulates the expression of PRDX4 gene in tumor cells at transcriptional level, but has no effect on the stability of PRDX4 mRNA.