髓样分化因子88与人卵巢癌紫杉醇耐药细胞系A2780/Taxol耐药性相关  

The relationship between MyD88 and paclitaxel-resistance of A2780/Taxol cell line

作　　者：邹冬玲[1] 李少林[1] 袁梨[1] 周琦[1] 

机构地区：[1]重庆医科大学基础医学院放射医学教研室,重庆400031

出　　处：《基础医学与临床》2013年第5期519-524,共6页Basic and Clinical Medicine

基　　金：国家自然科学基金(81071812)

摘　　要：目的本研究希望通过外源改变MyD88的表达,明确其与紫杉醇耐药的相关性,检测MyD88对细胞生物学活性的影响。方法通过在A2780/Taxol细胞中敲低和过表达MyD88后,利用real-time PCR和Western blot分别从mRNA和蛋白质水平检测MyD88的表达变化;CCK-8法检测细胞转染前后对紫杉醇耐药性的变化,流式技术检测MyD88对细胞周期和凋亡的影响。结果敲低MyD88表达水平,耐药细胞系A2780/Taxol对紫杉醇的耐药性明显降低(P<0.01),抗凋亡能力减弱(P<0.01);过表达MyD88后,细胞对紫杉醇耐药性增加(P<0.05)。结论抑制卵巢癌细胞中MyD88的表达,能促进耐药细胞系对紫杉醇的敏感性,为临床卵巢癌耐药患者以MyD88为靶向的基因治疗提供了新思路和手段。Objective To make clear the relationship between MyD88 and the resistance of ovarian cancer cell to paclitaxel. Methods After knocking-down and over-expressing MyD88 in A2780/Taxol cell line, qRT-PCR and Western blot were performed to test the expression change of MyD88 on mRNA and protein levels compared with control group, respectively. CCK-8 assay was applied to detect the change of resistance to paclitaxel in A2780/Tax- ol cells. Flow cytometry was performed to test the affection to Cell cycle and apoptosis of A2780/Taxol cell line. Re- sults By means of inhibiting MyD88, we observed that resistance of A2780/Taxol to paclitaxel declined obviously, and anti-apoptotic significantly weakened. Inversely, over-expression of MyD88 increased cells resistance to pacli- taxel. Conclusions Down-regulation of MyD88 increases sensitivity of ovarian cancer cell to paclitaxel, which pro- vide new ideas and targets of gene therapy for the clinical treatment of ovarian cancer resistant patients.

关 键 词：卵巢癌 紫杉醇耐药 MYD88 

分 类 号：R737.31[医药卫生—肿瘤]