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E-Cadherin mediates MMP down-regulation in highly invasive bronchial tumor cells.

Abstract : The disorganization of E-cadherin/catenin complexes and the overexpression of matrix metalloproteinases (MMPs) are frequently involved in the capacity of epithelial cells to acquire an invasive phenotype. The functional link between E-cadherin and MMPs was studied by transfecting invasive bronchial BZR tumor cells with human E-cadherin cDNA. Using different in vitro (cell dispersion, modified Boyden chamber) and in vivo assays (human airway epithelial xenograft), we showed that E-cadherin-positive clones displayed a decrease of invasive abilities. As shown by immunoprecipitation, the re-expressed E-cadherin was able to sequestrate one part of free cytoplasmic beta-catenin in BZR cells. The decrease of beta-catenin transcriptional activity in E-cadherin-transfected clones was demonstrated using the TOP-FLASH reporter construct. Finally, we observed a decrease of MMP-1, MMP-3, MMP-9, and MT1-MMP, both at the mRNA and at the protein levels, in E-cadherin-positive clones whereas no changes in MMP-2, TIMP-1, or TIMP-2 were observed when compared with control clones. Moreover, zymography analysis revealed a loss of MMP-2 activation ability in E-cadherin-positive clones treated with the concanavalin A lectin. These data demonstrate a direct role of E-cadherin/catenin complex organization in the regulation of MMPs and suggest an implication of this regulation in the expression of an invasive phenotype by bronchial tumor cells.
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Contributor : Philippe Birembaut Connect in order to contact the contributor
Submitted on : Thursday, May 24, 2007 - 9:57:28 AM
Last modification on : Wednesday, November 3, 2021 - 2:56:48 PM


  • HAL Id : inserm-00149014, version 1
  • PUBMED : 12875984



Béatrice Nawrocki-Raby, Christine Gilles, Myriam C. Polette, Corinne Martinella-Catusse, Noël Bonnet, et al.. E-Cadherin mediates MMP down-regulation in highly invasive bronchial tumor cells.. American Journal of Pathology, American Society for Investigative Pathology, 2003, 163 (2), pp.653-61. ⟨inserm-00149014⟩



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