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Transactivation of vimentin by beta-catenin in human breast cancer cells.

Abstract : The cytoplasmic and nuclear redistribution of beta-catenin and the de novo expression of vimentin are frequently involved in the epithelial-to-mesenchymal transition associated with increased invasive/migratory properties of epithelial cells. Because beta-catenin can act as a coactivator of transcription through its binding to the T-cell factor (TCF)/lymphoid enhancer factor 1 transcription factor family, we have explored the possibility that beta-catenin/TCF could directly transactivate vimentin. We first compared vimentin expression in relation with the localization of beta-catenin in eight breast cancer cell lines displaying various degrees of invasiveness and in a model of cell migration using human mammary MCF10A cells. We could thus show a cytoplasmic and/or nuclear distribution of beta-catenin in invasive/migratory cells expressing vimentin, but not in noninvasive/stationary vimentin-negative cell lines. In addition, the human vimentin promoter was found to be up-regulated by beta-catenin and TCF-4 cotransfection. Varying with the cellular background, a diminution of this up-regulation was observed when the putative beta-catenin/TCF binding site of the vimentin promoter was mutated. Our results therefore demonstrate that the vimentin promoter is a target of the beta-catenin/TCF pathway and strongly suggest an implication of this regulation in epithelial cell migration/invasion.
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https://www.hal.inserm.fr/inserm-00149065
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Submitted on : Wednesday, September 22, 2010 - 2:13:58 PM
Last modification on : Wednesday, August 30, 2017 - 1:13:29 AM
Long-term archiving on: : Thursday, December 23, 2010 - 2:28:42 AM

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  • HAL Id : inserm-00149065, version 1
  • PUBMED : 12750294

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Christine Gilles, Myriam Polette, Mélanie Mestdagt, Béatrice Nawrocki-Raby, Philippe Ruggeri, et al.. Transactivation of vimentin by beta-catenin in human breast cancer cells.. Cancer Research, American Association for Cancer Research, 2003, 63 (10), pp.2658-64. ⟨inserm-00149065⟩

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