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Research ArticleArticle

Involvement of Nuclear Factor κB in c-Myc Induction by Tubulin Polymerization Inhibitors

V. Bourgarel-Rey, S. Vallee, O. Rimet, S. Champion, D. Braguer, A. Desobry, C. Briand and Y. Barra
Molecular Pharmacology May 2001, 59 (5) 1165-1170; DOI: https://doi.org/10.1124/mol.59.5.1165
V. Bourgarel-Rey
Unité Mixte de Recherche Centre National de la Recherche Scientifique 6032, Faculté de Pharmacie, Marseille, France
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S. Vallee
Unité Mixte de Recherche Centre National de la Recherche Scientifique 6032, Faculté de Pharmacie, Marseille, France
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O. Rimet
Unité Mixte de Recherche Centre National de la Recherche Scientifique 6032, Faculté de Pharmacie, Marseille, France
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S. Champion
Unité Mixte de Recherche Centre National de la Recherche Scientifique 6032, Faculté de Pharmacie, Marseille, France
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D. Braguer
Unité Mixte de Recherche Centre National de la Recherche Scientifique 6032, Faculté de Pharmacie, Marseille, France
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A. Desobry
Unité Mixte de Recherche Centre National de la Recherche Scientifique 6032, Faculté de Pharmacie, Marseille, France
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C. Briand
Unité Mixte de Recherche Centre National de la Recherche Scientifique 6032, Faculté de Pharmacie, Marseille, France
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Y. Barra
Unité Mixte de Recherche Centre National de la Recherche Scientifique 6032, Faculté de Pharmacie, Marseille, France
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Abstract

We showed previously that microtubule disassembly by vinblastine induces the proto-oncogene c-myc in epithelial mammary HBL100 cells (Bourgarel-Rey et al., 2000). In this study, we demonstrate that vinblastine treatment in these cells, in contrast to what was observed with the colon adenocarcinoma cell line HT29-D4, activated the transcription factor NFκB, which has been involved in c-myc regulation. The microtubule disassembly also induced IκB degradation. Using transient transfection analysis, we show that thetrans-activation of c-myc by vinblastine was decreased when NFκB binding sites on c-myc promoter were mutated. Additionally, we demonstrate that microtubule dissolutiontrans-activated a thymidine kinase-CAT construct containing an NFκB binding site at −1180 to −1080 bp relative to the P1 promoter. Thus, vinblastine up-regulates the enhancer activity of the NFκB binding site. These results suggest that microtubule disassembly induced by vinblastine can trans-activate the c-myc oncogene through NFκB. Taking into consideration the paradoxical roles of both c-myc and NFκB in proliferation or apoptosis, this data reveals the complex action mechanism of this microtubule interfering agent.

Footnotes

    • Received November 1, 2000.
    • Accepted February 5, 2001.
  • Send reprint requests to: Pr. Yves Barra, Faculté de Pharmacie, 27 Bd Jean Moulin, 13005 Marseille, France. E-mail:yves.barra{at}pharmacie.univ-mrs.fr

  • V.B.-R. and S.B. contributed equally to this work

  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 59 (5)
Molecular Pharmacology
Vol. 59, Issue 5
1 May 2001
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Research ArticleArticle

Involvement of Nuclear Factor κB in c-Myc Induction by Tubulin Polymerization Inhibitors

V. Bourgarel-Rey, S. Vallee, O. Rimet, S. Champion, D. Braguer, A. Desobry, C. Briand and Y. Barra
Molecular Pharmacology May 1, 2001, 59 (5) 1165-1170; DOI: https://doi.org/10.1124/mol.59.5.1165

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Research ArticleArticle

Involvement of Nuclear Factor κB in c-Myc Induction by Tubulin Polymerization Inhibitors

V. Bourgarel-Rey, S. Vallee, O. Rimet, S. Champion, D. Braguer, A. Desobry, C. Briand and Y. Barra
Molecular Pharmacology May 1, 2001, 59 (5) 1165-1170; DOI: https://doi.org/10.1124/mol.59.5.1165
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