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pubmed-article:11082419pubmed:abstractTextDaunomycin is a potent inducer of p53 and NF-kappaB transcription factors. It is also able to increase the amount of the p21 cyclin-dependent kinase inhibitor. The human p21 promoter harbors p53-responsive elements and an NF-kappaB binding site. We demonstrated, in human breast and colon carcinoma cells, the binding of NF-kappaB dimers to the kappaB site and the transcriptional activation of the human p21 promoter by daunomycin and by NF-kappaB subunits, thereby confirming the functionality of this kappaB binding site. However, using different tumor cell lines where p53 or NF-kappaB was inactive, we showed that p21 activation and cell cycle arrest induced by daunomycin was p53-dependent and NF-kappaB-independent, whereas daunomycin-induced apoptosis was p53- and NF-kappaB-independent.lld:pubmed
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pubmed-article:11082419pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:11082419pubmed:articleTitleRoles of nuclear factor-kappaB, p53, and p21/WAF1 in daunomycin-induced cell cycle arrest and apoptosis.lld:pubmed
pubmed-article:11082419pubmed:affiliationLaboratory of Medical Chemistry and Medical Oncology, University of Liège, Sart-Tilman, Liège, Belgium.lld:pubmed
pubmed-article:11082419pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11082419pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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