卵巢癌耐药细胞株体外模型的建立及相关研究  

作　　者：张晓菁[1] 姚晓奕[1] 常玉华[1] 贾艳敏[1] 

机构地区：[1]山东省交通医院,山东济南250031

出　　处：《山东医药》2005年第32期3-5,共3页Shandong Medical Journal

基　　金：山东省交通科技计划基金资助(2005-Y026)

摘　　要：目的探讨人卵巢癌细胞多药耐药(MDR)的发生机制。方法以浓度梯度诱导法建立卵巢癌阿霉素(ADM)耐药细胞亚株OVCAR/AR。人多药耐药基因(MDR1)转染OVCAR-3细胞建立多药耐药亚株OV-CAR/MDR细胞。流式细胞术检测P-糖蛋白(P-gp)的表达,罗丹明试验检测P-gp的药物转运功能;MTT法检测细胞对化疗药的抵抗性。结果成功地建立了人卵巢癌MDR细胞株OVCAR/AR和OVCAR/MDR。与亲代细胞OVCAR-3相比,两株耐药细胞P-gp的表达水平显著增加,转运功能增强。OVCAR/AR细胞对ADM、泰素(TAX)和顺铂(DDP)产生交叉耐药,而OVCAR/MDR细胞只对前两者产生耐药。结论OVCAR/AR细胞和OVCAR/MDR细胞具有典型的MDR表型,其机制主要是MDR1基因过度表达致细胞内药物浓度减少。Objective： To explore the development of ovarian carcinoma multidrug resistant （MDR） and possible ways to overcome it. Methods： OVCAR/AR was established by stepwise inducement. Another mutidrug-resistant human ovarian cancer cell subline OVCAR/MDR was established by transfecting human multidrug resistant gene （MDR1） into OVCAR-3 cells. Flow cytometry （FCM） was performed to assess the expression of p-glycoprotein （P-gp）. The transporting function of P-gp was determined by Rhodamine assay. Multidrug resistant to anticancer agents was evaluated by MTT assay. Results：Basal P-gp expression level and transporting function of P-gp in OVCAR/AR and OVCAR/MDR cells was higher than that in parent cell line OVCAR-3. OVCAR/AR and OVCAR/MDR cells displayed much higher resistance to Adriamycin and Paclitaxel. Conclusion：The typical multidrug resistant phenotypes showed in OVCAR/AR and OVCAR/MDR ceils possibly was caused by overexpression of MDR-1 gene.

关 键 词：卵巢肿瘤 细胞株 多药耐药 

分 类 号：R733.31[医药卫生—肿瘤]