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MCF7人乳腺癌细胞系中阿霉素和米托蒽醌耐药变体药物蓄积减少的不同机制。

Different mechanisms of decreased drug accumulation in doxorubicin and mitoxantrone resistant variants of the MCF7 human breast cancer cell line.

作者信息

Taylor C W, Dalton W S, Parrish P R, Gleason M C, Bellamy W T, Thompson F H, Roe D J, Trent J M

机构信息

Department of Internal Medicine, Arizona Cancer Center, University of Arizona, Tucson 85724.

出版信息

Br J Cancer. 1991 Jun;63(6):923-9. doi: 10.1038/bjc.1991.202.

DOI:10.1038/bjc.1991.202
PMID:1676902
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1972545/
Abstract

We selected two drug resistant variants of the MCF7 human breast cancer cell line by chronic in vitro exposure to doxorubicin (MCF7/D40 cell line) and mitoxantrone (MCF7/Mitox cell line), respectively. The cell lines are similar in growth characteristics including doubling time, DNA synthetic phase and cell size. Resistance to mitoxantrone conferred only partial resistance to doxorubicin; whereas resistance selected for doxorubicin appeared to confer complete resistance to mitoxantrone. Both agents selected for cross resistance to the Vinca alkaloids. MCF7/D40 cells display a classic-multi-drug resistance phenotype with expression of P-glycoprotein, decreased drug accumulation relative to the parental line and reversal of drug accumulation and drug resistance by verapamil. MCF7/Mitox cells likewise display resistance to multiple drugs, but in contrast to MCF7/D40 cells do not express P-glycoprotein by immunoblot or RNA blot analysis. Net drug accumulation in MCF7/Mitox cells was decreased relative to the parental cells but there was no selective modulation of drug accumulation or in vitro drug resistance by the addition of verapamil. Efflux of mitoxantrone was enhanced in both the MCF7/D40 and MCF7/Mitox cell lines relative to the MCF7/S cell line. We conclude that the two drug resistant cell lines have different mechanisms of decreased drug accumulation.

摘要

我们分别通过长期体外暴露于阿霉素（MCF7/D40细胞系）和米托蒽醌（MCF7/Mitox细胞系），筛选出了MCF7人乳腺癌细胞系的两种耐药变体。这些细胞系在生长特性方面相似，包括倍增时间、DNA合成期和细胞大小。对米托蒽醌的耐药性仅赋予了对阿霉素的部分耐药性；而因阿霉素筛选出的耐药性似乎赋予了对米托蒽醌的完全耐药性。两种药物均筛选出了对长春花生物碱的交叉耐药性。MCF7/D40细胞表现出经典的多药耐药表型，具有P-糖蛋白表达，相对于亲代细胞系药物蓄积减少，且维拉帕米可逆转药物蓄积和耐药性。MCF7/Mitox细胞同样表现出对多种药物的耐药性，但与MCF7/D40细胞不同的是，通过免疫印迹或RNA印迹分析未检测到P-糖蛋白表达。相对于亲代细胞，MCF7/Mitox细胞中的药物净蓄积减少，但添加维拉帕米后未对药物蓄积或体外耐药性产生选择性调节作用。相对于MCF7/S细胞系，MCF7/D40和MCF7/Mitox细胞系中米托蒽醌的外排均增强。我们得出结论，这两种耐药细胞系减少药物蓄积的机制不同。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8000/1972545/23d53f8ab20d/brjcancer00214-0095-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8000/1972545/2c9ae0f67b4b/brjcancer00214-0095-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8000/1972545/23d53f8ab20d/brjcancer00214-0095-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8000/1972545/2c9ae0f67b4b/brjcancer00214-0095-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8000/1972545/23d53f8ab20d/brjcancer00214-0095-b.jpg

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