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

We showed previously that microtubule disassembly by vinblastine induces the proto-oncogene c-myc in epithelial mammary HBL100 cells ([Bourgarel-Rey et al., 2000][1]). 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 the trans -activation of c-myc by vinblastine was decreased when NFκB binding sites on c-myc promoter were mutated. Additionally, we demonstrate that microtubule dissolution trans -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. [1]: #ref-9

• Publication year

  2001

• Venue

  Molecular Pharmacology

• Publication date

  2001-05-01

• Fields of study

  Biology

• Identifiers
  DOI 10.1124/MOL.59.5.1165
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

• No claims are published for this paper.

• No concepts are published for this paper.

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