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具有突变拓扑异构酶IIα的氨吖啶耐药人白血病细胞系中拓扑异构酶IIβ缺失。

Absence of topoisomerase IIbeta in an amsacrine-resistant human leukemia cell line with mutant topoisomerase IIalpha.

作者信息

Herzog C E, Holmes K A, Tuschong L M, Ganapathi R, Zwelling L A

机构信息

University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.

出版信息

Cancer Res. 1998 Dec 1;58(23):5298-300.

PMID:9850052
Abstract

Numerous chemotherapeutic agents act via stabilization of a topoisomerase (topo) II-DNA complex. HL-60/AMSA, a human leukemia cell line, is resistant to intercalator-mediated DNA complex formation and cytotoxicity. HL-60/AMSA contains a mutant form of topo IIalpha that was thought to explain this resistance. However, our present data show that expression of topo IIbeta RNA in HL-60/AMSA is only 10% of that in HL-60, and topo IIbeta protein levels are undetectable. Southern analysis of topo IIbeta shows no differences in gene dosage between the two cell lines but does show differences in the restriction patterns. These data suggest that decreased topo IIbeta expression may contribute to the intercalator resistance of HL-60/AMSA cells.

摘要

许多化疗药物通过稳定拓扑异构酶（topo）II-DNA复合物发挥作用。人白血病细胞系HL-60/AMSA对嵌入剂介导的DNA复合物形成和细胞毒性具有抗性。HL-60/AMSA含有拓扑异构酶IIα的突变形式，曾被认为可以解释这种抗性。然而，我们目前的数据表明，HL-60/AMSA中拓扑异构酶IIβRNA的表达仅为HL-60中的10%，且无法检测到拓扑异构酶IIβ蛋白水平。对拓扑异构酶IIβ进行的Southern分析显示，这两种细胞系之间的基因剂量没有差异，但限制酶切图谱存在差异。这些数据表明，拓扑异构酶IIβ表达的降低可能导致HL-60/AMSA细胞对嵌入剂产生抗性。

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