摘要
目的探索卵巢癌细胞对TRAIL诱导凋亡耐药抵抗的机制。方法分别选择12.5、25、50、100ng/mL的人重组TRAIL蛋白作用于卵巢癌细胞3AO和CAOV3,在18、24、48、72h时间点收集细胞,MTT法检测细胞的生长抑制率;原位末端标记法(TUNEL)观察凋亡细胞;流式细胞仪(FCM)检测细胞的凋亡率;Western blot检测凋亡抑制蛋白c-FLIP蛋白表达的水平。结果 TRAIL抑制了3AO和CAOV3细胞的生长增殖,24h3AO、CAOV3细胞的生长抑制率分别为28%、10%,并且TRAIL增多可诱导细胞凋亡,24h的3AO细胞凋亡率(8.5%)明显高于CAOV3(5.5%)。CAOV3细胞中c-FLIP蛋白的表达水平高于3AO细胞。结论 c-FLIP蛋白是卵巢癌细胞对TRAIL耐药抵抗的一种重要调控蛋白。
Objective To explore the mechanism of drug resistance of ovarian cancer cells to TRAIL-induced apoptosis; Methods We collected 3AO cells and CAOV3 cells, respectively, at 18, 24, 48 and 72 hour under 12.5, 25, 50 and 100 ng/mL concentrations of TRAIL. The rate of cell growth inhibition was checked by methyl thiazolyl tetrazolium （MTT） assay to evaluate the effect of TRAIL. Morphology of apoptotic cells was observed by TdT-mediated-dUTP nick end labeling （TUNEL）. The apoptosis rate was detected by flow cytometry （FCM） and C- FLIP protein was determined by Western blotting. Results TRAIL inhibited the growth of 3AO and CAOV3 cells. The rate of growth inhibition at 24 hour was 28% in 3AO cells and 10% in CAOV3 cells. TRAIL induced apoptosis of cells. The apoptosis rate at 24 hour was 8.5% in 3AO cells, which was higher than 5.5% in CAOV3 cells. The expression level of C-FLIP protein was higher in CAOV3 cells than in 3AO cells. Conclusion C-FLIP protein is an important protein that regulates drug resistance of ovarian cancer cells to TRAIL-induced apoptosis.
出处
《西安交通大学学报（医学版）》
CAS
CSCD
北大核心
2014年第3期380-384,共5页
Journal of Xi’an Jiaotong University（Medical Sciences）
基金
陕西省自然科学基础研究计划资助项目(No.2013JM4058)
陕西省教育厅项目(No.11JKO724)
西安医学院科研项目(No.10FC07)
西安医学院附属医院科研项目(No.XYFY10-11)~~
