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Autoregulation of E-cadherin expression by cadherin-cadherin interactions: the roles of beta-catenin signaling, Slug, and MAPK.

Abstract : Transcriptional repression of E-cadherin, characteristic of epithelial to mesenchymal transition, is often found also during tumor cell invasion. At metastases, migratory fibroblasts sometimes revert to an epithelial phenotype, by a process involving regulation of the E-cadherin-beta-catenin complex. We investigated the molecular basis of this regulation, using human colon cancer cells with aberrantly activated beta-catenin signaling. Sparse cultures mimicked invasive tumor cells, displaying low levels of E-cadherin due to transcriptional repression of E-cadherin by Slug. Slug was induced by beta-catenin signaling and, independently, by ERK. Dense cultures resembled a differentiated epithelium with high levels of E-cadherin and beta-catenin in adherens junctions. In such cells, beta-catenin signaling, ErbB-1/2 levels, and ERK activation were reduced and Slug was undetectable. Disruption of E-cadherin-mediated contacts resulted in nuclear localization and signaling by beta-catenin, induction of Slug and inhibition of E-cadherin transcription, without changes in ErbB-1/2 and ERK activation. This autoregulation of E-cadherin by cell-cell adhesion involving Slug, beta-catenin and ERK could be important in tumorigenesis.
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https://www.hal.inserm.fr/inserm-00148047
Contributor : Yves Le Ster <>
Submitted on : Wednesday, May 23, 2007 - 8:58:02 AM
Last modification on : Thursday, October 15, 2020 - 2:42:03 PM
Long-term archiving on: : Thursday, April 8, 2010 - 5:18:30 PM

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Maralice Conacci-Sorrell, Inbal Simcha, Tamar Ben-Yedidia, Janna Blechman, Pierre Savagner, et al.. Autoregulation of E-cadherin expression by cadherin-cadherin interactions: the roles of beta-catenin signaling, Slug, and MAPK.. Journal of Cell Biology, Rockefeller University Press, 2003, 163 (4), pp.847-57. ⟨10.1083/jcb.200308162⟩. ⟨inserm-00148047⟩

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