COX-2基因在紫杉醇/卡铂致卵巢癌细胞凋亡中的作用及机制研究

摘要

目的 探讨环氧合酶-2(COX-2)在紫杉醇/卡铂致卵巢癌细胞凋亡中的作用及机制. 方法 以卵巢癌CAOV-3细胞系,卵巢癌组织及其相应的癌旁正常组织为材料,采用实时荧光定量PCR和免疫印迹法分别检测COX-2基因mRNA和蛋白质表达;流式细胞术检测CAOV-3细胞的凋亡情况,同时采用透射电镜观察细胞的超微结构变化. 结果 COX-2基因在卵巢癌组织中的表达明显高于其对应的癌旁正常组织(P<0.01);与紫杉醇/卡铂组比较,转染紫杉醇/卡铂+pCMV-COX-2组卵巢癌细胞凋亡率明显减少(P<0.01),且细胞超微结构未发生显著改变. 结论 COX-2基因在紫杉醇/卡铂治疗卵巢癌中发挥重要作用,其有望成为卵巢癌治疗的分子新靶标.%Objective To investigate the role of cyclooxygenase-2 (COX-2) in the apoptosis of ovarian cancer cells induced by paclitaxel/carboplatin.Methods In ovarian cancer cell line CAOV-3, ovarian cancer tissue, and the corresponding adjacent normal tissue, the expression of COX-2 mRNA gene and protein was explored by Real-time PCR and Western blot, meanwhile, CAOV-3 apoptosis was detected by flow cytometry.Its ultra-microstructure changes were observed by transmission electron microscope.Results The expression of COX-2 mRNA gene was significantly higher in ovarian cancer tissue than that in adjacent normal tissue (P< 0.01).Compared with paclitaxel/carboplatin group, the apoptosis rate of ovarian cancer cells was obviously reduced(P< 0.01).And the morphological changes of apoptosis were not significant in paclitaxel/carboplatin+pCMV-COX-2 group.Conclusions Cox-2 plays an important role in ovarian cancer cell apoptosis induced by paclitaxel/carboplatin, and may be a new therapy molecular target.