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Vol. 295, Issue 3, 870-878, December 2000

Roles of Nuclear Factor-kappa B, p53, and p21/WAF1 in Daunomycin-Induced Cell Cycle Arrest and Apoptosis1

Anne-Cécile Hellin, Mohamed Bentires-Alj, Myriam Verlaet, Valérie Benoit, Jacques Gielen, Vincent Bours and Marie-Paule Merville

Laboratory of Medical Chemistry and Medical Oncology (A.-C.H., M.B.-A., V.Be., J.G., V.Bo., M.-P.M.) and Laboratory of Pathological Anatomy (M.V.), University of Liège, Sart-Tilman, Liège, Belgium

Daunomycin is a potent inducer of p53 and NF-kappa B 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-kappa B binding site. We demonstrated, in human breast and colon carcinoma cells, the binding of NF-kappa B dimers to the kappa B site and the transcriptional activation of the human p21 promoter by daunomycin and by NF-kappa B subunits, thereby confirming the functionality of this kappa B binding site. However, using different tumor cell lines where p53 or NF-kappa B was inactive, we showed that p21 activation and cell cycle arrest induced by daunomycin was p53-dependent and NF-kappa B-independent, whereas daunomycin-induced apoptosis was p53- and NF-kappa B-independent.

1 This research was supported by grants from Télévie, the National Fund for Scientific Research, and the "Centre Anti-Cancéreux" (University of Liège, Belgium). A.-C.H. is a Research Assistant at the National Fund for Scientific Research (Belgium). V.Bo. is a Senior Research Associate and M.-P.M. is a Research Associate at the National Fund for Scientific Research (Belgium).

0022-3565/00/2953-0870$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 2000 by The American Society for Pharmacology and Experimental Therapeutics


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