人结肠癌HCTv2000细胞系耐药机制的初步研究  

Preliminary Study on Mechanism of Drug Resistance in HumanColon Cancer Cell Line HCTv2000

作　　者：张晓红[1] 诸亚君[1] 籍秀娟[2] 李学汤[1] 

机构地区：[1]中国医学科学院肿瘤研究所,北京100021 [2]中国医学科学院药物研究所,北京100050

出　　处：《浙江肿瘤》1996年第1期23-26,共4页

基　　金：本课题为国家"八五"科技攻关项目

摘　　要：HCTv2000是人结肠癌HCT-8细胞系经长春新碱选择而建立的耐药系。该系细胞对抗P-糖蛋白单抗呈阳性反应。编码P-精蛋白的多向耐药基因mdrl未见扩增或重排，但mdrlmRNA过度表达。异博定使细胞内3H-长春新碱蓄积增多，可部分逆转耐药。据此认为，mdrl基因的转录性激活是HCTv2000细胞耐药的重要原因，但有其他机制参与。The HCTv2000 cells were selected with increasing concentrations of vincristine from a human coloncancer line (HCT-8). In the present study, the mechanism of drug resisbocepf HCTv2000 cells reintive to the mdrl gene was observed. Immunocytochemical staining showed a poaitive response to monoclonal antibodies (JSB-1and MRK-16) against P-glycoptotein (P-GP) encoded by the mdrl gene. A high level of mdrl mRNA was found bymeans of Slot blotting and Northern blotting. However, no evidence of mdrl gene arnplification or rearrangementwas detectal. Verapamil increased the accumulation of 3H-vincristine indse the cells but did not appear to reverse drug resistance to vincrithee completely, demonstrating thet there ndght be other mechanism(8) also involvedin the HCTv2000 cells.

关 键 词：结肠癌 细胞系 耐药 MDRL基因 P-GP 

分 类 号：R735.35[医药卫生—肿瘤]