对顺铂耐药的L1210小鼠白血病细胞亚系中甲氨蝶呤耐药机制的研究。
Investigations on the mechanisms of methotrexate resistance in a cisplatin-resistant L1210 murine leukemia cell subline.
作者信息
Wroblewski D H, Bhushan A, Xuan Y, Brinton B T, Tritton T R, Hacker M P
机构信息
Department of Pharmacology, University of Vermont College of Medicine, Burlington 05405, USA.
出版信息
Cancer Chemother Pharmacol. 1996;37(4):337-42. doi: 10.1007/s002800050394.
We report a murine leukemia cell variant (L1210/DDP), selected for cisplatin (DDP) resistance, to be cross-resistant to methotrexate (MTX). Cross-resistance of L1210 cells to DDP and MTX has been observed by others, and has also been recorded in P388 murine leukemia and SSC-25 human squamous carcinoma cells. We demonstrated that MTX resistance is not due to dihydrofolate reductase (DHFR) gene amplification, increased DHFR enzyme activity or decreased MTX binding to the target enzyme. Of the mechanisms commonly proposed for MTX resistance, only differences in transport were observed when comparing sensitive (L1210/0) and resistant (L1210/DDP) cells. Our results suggest that MTX resistance in L1210/DDP cells is due to altered methotrexate uptake.
我们报告了一种为顺铂（DDP）耐药而筛选出的小鼠白血病细胞变体（L1210/DDP），它对甲氨蝶呤（MTX）也具有交叉耐药性。其他人已观察到L1210细胞对DDP和MTX存在交叉耐药性，并且在P388小鼠白血病细胞和SSC - 25人鳞状癌细胞中也有记录。我们证明，MTX耐药性并非由于二氢叶酸还原酶（DHFR）基因扩增、DHFR酶活性增加或MTX与靶酶的结合减少所致。在通常提出的MTX耐药机制中，比较敏感细胞（L1210/0）和耐药细胞（L1210/DDP）时，仅观察到转运方面的差异。我们的结果表明，L1210/DDP细胞中的MTX耐药性是由于甲氨蝶呤摄取改变所致。
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