AQP3在上皮型卵巢癌细胞卡铂耐药中的作用  

Effect of AQP3 on carboplatin resistance in epithelial ovarian cancer cells

作　　者：潘洁雪[1] 叶龙云[2] 

机构地区：[1]温州医科大学附属第一医院生殖医学中心,浙江温州325000 [2]温州医科大学附属第一医院,浙江温州325000

出　　处：《中国现代医生》2017年第15期27-29,F0003,共4页China Modern Doctor

基　　金：浙江省中医药管理局青年人才基金项目(2017ZQ020);浙江省医药卫生科技计划项目(2017KY462);浙江省温州市科技局项目(Y20160037)

摘　　要：目的探索上皮型卵巢癌细胞卡铂耐药的机制,为提高卵巢癌患者化疗效果提供前期基础。方法应用CCK8方法检测卵巢癌细胞对卡铂的IC50浓度,用Western blot方法检测卡铂处理后细胞上皮间质化转变(EMT)蛋白E-Cadherin和Vimentin表达情况,使用siRNA敲降AQP3后再观察卡铂对其作用。结果卵巢癌细胞系SKOV3与A2780的卡铂IC50分别为2.814μg/mL与1.516μg/mL,同时发现卡铂能诱导卵巢癌细胞发生EMT,基因芯片结果显示水通道蛋白AQP3显著上调,进一步敲降AQP3基因后,能显著减弱卡铂诱导卵巢癌细胞产生EMT的效果。结论 AQP3在卵巢癌细胞卡铂耐药机制中具有重要作用,降低AQP3的表达可以减弱卡铂诱导卵巢癌细胞上皮间质化转变的效果。Objective To discusa the mechanism of carboplatin resistance in epithelial ovarian cancer cells and to provide basis for improvement of chemotherarapy effect in patients with ovarian cancer. Methods The IC50 concentration of ovarian cancer cells towards carhoplatin was detected by CCKS, the expression of EMT proteins E-Cadherin and Vimentin after management of carboplatin was detected by Western blot, and the effect of carboplatin was observed again after AQP3 was knocked down by siRNA. Results The carboplatin IC50 was 2.814 μg/mL in SKOV3 ovarian cancer cell line and 1.516 μg/mL in A2780 line. Carboplatin could induce EMT in ovarian cancer ceils. As to the result of gene chip, AQP3 was significantly up-regulated. When AQP3 gene was knocked down, EMT effect induced by carboplatin in ovarian cancer ceils could be significantly reduced. Conclusion AQP3 has significant effect in the mechanisom of carboplatin resistance in ovarion cancer cells and reduction of the expression of AQP3 can reduce the EMT effect in ovarain cancer cells.

关 键 词：卵巢癌 卡铂 上皮间质化转变 水通道蛋白 

分 类 号：R737.31[医药卫生—肿瘤]