摘要
建立耐药肝癌细胞模型 7721/Adm并研究其生物学特性。方法 :应用人肝癌细胞株 7721(简称7721细胞株 ) ,采用阿霉素 (Adm)高浓度间歇诱导法 ,建立耐药人肝癌细胞模型 7721/Adm(简称7721/Adm细胞株 )。观察该细胞的生长规律 ;用MTT法检测该耐药细胞模型的多药耐药性 ;以流式细胞术检测该耐药模型细胞周期中的分布、细胞表面多药耐药基因 (mdr)的表达产物P 糖蛋白 (P gp)、多药耐药相关蛋白 (MRP)及谷胱甘肽硫转移系统 (GSH/GST)的表达等。结果 :1 经MTT法检测7721/Adm细胞较HCC 7721细胞的阿霉素半数抑制浓度 (IC50)增大99 9倍 ,并对多种抗癌药物产生耐药性。2 耐药细胞的倍增时间明显延长 ,S期细胞减少 ,G1、G2 期细胞增多。3 该耐药模型细胞表面多药耐药基因 (mdr)的表达产物P 糖蛋白 (P gp)、多药耐药相关蛋白 (MRP)有非常显著的升高 (P<0 01) ,P gp 表达为94 6 %、MRP表达为69 4% ,而谷胱甘肽硫转移系统 (GSH/GST)的表达无明显变化 (P>0 05)。结论 :7721/Adm细胞是一个明确的多药耐药模型 ;具有耐药细胞的基本生物学特性 :同亲本细胞相比 ,IC50提高99 9倍、倍增时间延长4 2倍、细胞内药物蓄积明显降低、细胞周期分布发生变化 ;其多药耐药性与P gp。
Objective: To establish human multidrug resistant hepatocellular carcinoma cell line (7721/Adm) and to investigate its characteristics Methods:Through intermittant exposure to high concentration ADM, human cell line (7721) was induced to form multidrug resistant hepatocellular carcinoma cell line(7721/Adm) The multidrug resistance of 7721/Adm to multianticancer agents was evaluated by MTT assay The distribution of its cell cycle, the expressions of P gp, multidrug resistance associated protein (MRP) and GSH/GST were detected by flow cytometry Results: ①7721/Adm was resistant to many anti tumor agents Its IC50 of ADM was 99 9 times higher than that of parent cell line 7721 and its drug resistance to ADM was 70～150 times higher against various antitumor agents than that of 7721 ②The doubling time of 7721/Adm prolonged, and the number of cells in S phasedecreased while those in G1 and G2 phase increased ③The expressions of P gp and MRP were enhanced significantly (94 6%and 69 4%respectively), but the expression of GSH/GST kept stable Conclusion: 1 We successfully established a multidrug resistant cell line(7721/Adm) which has the basic characteristics of drug resistance cells 2 Compared with its parent cell line7721, its IC50 increased 99 9 times, and its doubling time prolonged 4 6 times, drug accumulation decreased remarkably and distribution of its cell cycle changed 3 Its multidrug resistance was closely related to the overexpression of P gp and MRP
出处
《癌症》
SCIE
CAS
CSCD
北大核心
2000年第8期748-751,共4页
Chinese Journal of Cancer
基金
第四军医大学创新工程及陕西省攻关课题!(编号CX99A016)
