【摘要】 目的观察环氧化酶-2(COX-2)活性抑制后,人膀胱癌T24细胞中Survivin、Smad2、VEGFmRNA及其蛋白表达的变化,探讨COX-2及其特异性抑制剂尼美舒利(NIM)对人膀胱癌生物学行为影响的可能机制。方法体外培养的人膀胱癌T24细胞受终浓度为90μmol/L的NIM作用后,采用ELISA法检测细胞分泌PGE2变化,半定量RT-PCR法、WesternBlot法检测COX-2、Survivin、Smad2、VEGFmRNA及其蛋白表达变化。结果COX-2活性抑制后T24细胞分泌PGE2较对照组明显减少(P<0.05);实验组Survivin、VEGFmRNA及其蛋白表达较对照组减弱(P<0.05),Smad2mRNA及其蛋白表达增强(P<0.05),而COX-2mRNA及其蛋白表达无显著变化(P>0.05)。结论COX-2及其特异性抑制剂NIM可能通过PGE2调控凋亡负性调控基因Survivin、信号传导相关的Smad2基因及血管形成相关的VEGF基因的表达,进而影响膀胱癌的生物学行为。更多还原

【Abstract】 Objective To observe the change of Survivin, Smad2, VEGFmRNA and their protein in T24 cell lines by inhibiting activated COX-2 to investigate potential mechanism of COX-2 and the effect of selective COX-2 inhibitor nimesulide on the biological behavior of human bladder cancer. Methods The T24 cell line was cultured in vitro, and exposed to nimesulide （90μmol/L）. PGE₂ level was detected by ELISA. Expression of COX-2, Survivin, Smad2, VEGFmRNA and their protein was examined by semiquantitative reverse transcriptase-polyerase chain reaction（RT-PCR） and Western blot analysis. Results PGE₂ production, and the expression of survivin and VEGF decreased more in the experimental group than in the control group（P<0.05）. Expression of Smad2 increased in the experimental group（P>0.05）, but expression of COX-2 in T24 did not change. Conclusion COX-2 and the selective COX-2 inhibitor nimesulide may affect the biological behavoir of bladder cancer through regulating the expression of Survivin, Smad2, and VEGF by PGE₂.更多还原