Adriamycin activates NF-κB in human lung carcinoma cells by IκBα degradation

被引：14

作者：

Andriollo, M ^{[1
]}

Favier, A

Guiraud, P

机构：

[1] Univ Grenoble 1, Fac Pharm, CEA,LRC 8M, Lab Biol Stress Oxydant,MNERT JE538, Grenoble, France

[2] CEA, SCIB, DRFMC, Lab Le Sions Acides Nucl, Grenoble, France

来源：

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS | 2003年 / 413卷 / 01期

关键词：

adriamycin; NF-kappa B; oxidative stress; GLC(4) cells; topoisomerase II; apoptosis; Spl;

D O I：

10.1016/S0003-9861(03)00114-0

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The aim of this study was to investigate the effect of adriamycin (ADR) in signaling activation of NF-kappaB in ADR-sensitive and -resistant GLC(4) human small-cell lung carcinoma. ADR activated NF-kappaB only in ADR-sensitive GLC(4) cells in a time- and dose-dependant manner by stimulating IkappaBalpha degradation after 4 h. Activation of NF-kappaB in response to tumor necrosis factor was intact in both cell lines. Topoisomerase II, a target for a number of chemotherapeutic agents, was depleted in both types of GLC4 cells after ADR treatment, suggesting the stabilization of transient DNA-topoisomerase II complexes. Another transcription factor, Sp1, was activated by ADR, demonstrating the nonspecificity of NF-kappaB activation in ADR-sensitive GLC(4) cells. These findings indicated that resistance to ADR in ADR-sensitive GLC(4) cells did not involve the NF-kappaB transcription factor. (C) 2003 Elsevier Science (USA). All rights reserved.

引用

页码：75 / 82

页数：8

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