MECHANISMS INVOLVED IN THE DEVELOPMENT OF ADRIAMYCIN RESISTANCE IN HUMAN LEUKEMIC-CELLS

被引：18

作者：

KATO, S ^{[1
]}

IDEGUCHI, H ^{[1
]}

MUTA, K ^{[1
]}

NISHIMURA, J ^{[1
]}

NAWATA, H ^{[1
]}

机构：

[1] KYUSHU UNIV,FAC MED,DEPT INTERNAL MED 3,3-1-1 MAIDASHI,HIGASHI KU,FUKUOKA 812,JAPAN

来源：

LEUKEMIA RESEARCH | 1990年 / 14卷 / 06期

关键词：

adriamycin; DNA topoisomerase II; glutathione-s-transferase; human leukemic cells; Multidrug resistance; P-glycoprotein;

D O I：

10.1016/0145-2126(90)90009-X

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

We have developed three adriamycin (ADR)-resistant K562 sublines with different degrees of resistance. These sublines show a decreased accumulation and an increased efflux of ADR in proportion to the degree of resistance. Two membrane proteins (mol. wt 170,000 and 230,000) reactive with monoclonal antibody againstP-glycoprotein were highly expressed in both the K562/ADR200 and the K562/ADR500 subline. Less resistant K562/ADR80 cells contained only small amounts of mol. wt 230,000 protein. Thus, the level ofP-glycoprotein expression was not proportionate to the degree of ADR efflux. Verapamil treatment could not completely reverse ADR resistance. No significant change of glutathione-s-transferase activity nor in the level of DNA topoisomerase II was detected in resistant sublines. In our sublines it seems thatP-glycoprotein is one of the mechanisms for resistance, but additional mechanisms may be involved. © 1990 Pergamon Press plc.

引用

页码：567 / &

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