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

作者: V. Bourgarel-Rey , S. Vallee , O. Rimet , S. Champion , D. Braguer

DOI: 10.1124/MOL.59.5.1165

关键词:

摘要: 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 treatment these cells, contrast to what was observed with colon adenocarcinoma cell line HT29-D4, activated transcription factor NFκB, which has been involved regulation. The also induced IκB degradation. Using transient transfection analysis, show trans -activation of decreased when NFκB binding sites on promoter were mutated. Additionally, dissolution -activated a thymidine kinase-CAT construct containing an site at −1180 −1080 bp relative P1 promoter. Thus, up-regulates enhancer activity site. These results suggest can -activate oncogene through NFκB. Taking into consideration paradoxical roles both and proliferation or apoptosis, data reveals complex action mechanism interfering agent. [1]: #ref-9

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