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J. Biol. Chem., Vol. 281, Issue 6, 3560-3568, February 10, 2006

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E-cadherin-dependent Transcriptional Control of Apolipoprotein A-IV Gene Expression in Intestinal Epithelial Cells

A ROLE FOR THE HEPATIC NUCLEAR FACTOR 4^*

Gregory Peignon, Sophie Thenet, Cyrille Schreider, Stéphane Fouquet, Agnès Ribeiro, Elizabeth Dussaulx, Jean Chambaz, Philippe Cardot, Martine Pinçon-Raymond, and Johanne Le Beyec²

From the Université Pierre et Marie Curie UMRS 505, Paris, F-75006 France, INSERM, UMRS 505, F-75006 Paris, France, and Laboratoire de Pharmacologie Cellulaire et Moléculaire, Ecole Pratique des Hautes Etudes, F-75006 Paris, France

Cell-matrix and cell-cell adhesion play a central role in the control of cell proliferation, differentiation, and gene expression. Integrins and E-cadherin are the key components involved in these processes in epithelial cells. We recently showed that integrin-dependent adhesion to the extracellular matrix reinforces the formation of E-cadherin-actin complexes inducing the polarization of Caco-2 enterocytes and increases the expression of a marker of enterocyte differentiation, the apolipoprotein A-IV (apoA-IV) gene. By impairing or enhancing E-cadherin-dependent cell adhesion, we demonstrate in the present study its involvement in the transcriptional activation of the apoA-IV gene in Caco-2 cells. This control requires the regulatory sequence that we have previously identified as necessary and sufficient to drive and restrict apoA-IV gene expression in enterocytes in vivo. Furthermore, using chimeric E-cadherin-Fc homophilic ligand-coated surfaces, we show that a direct activation of E-cadherin triggers the transcriptional activation of the apoA-IV promoter. Finally, E-cadherin-dependent cell-cell adhesion controls the nuclear abundance of the transcription factor hepatic nuclear factor 4, which is involved in the enterocyte-specific expression of apoA-IV gene. Altogether, our results suggest that E-cadherin controls enterocyte-specific expression of genes, such as the apoA-IV gene, through the control of hepatic nuclear factor 4 nuclear abundance.

Received for publication, June 10, 2005 , and in revised form, November 17, 2005.

^* This work was supported by Université Paris VI, INSERM, and CNRS. This work was performed using IFR 58 facilities. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Recipient of a fellowship from Ministère de l'Enseignement Supérieur et de la Recherche.

² To whom correspondence should be addressed: UMR505 INSERM-Université Pierre and Marie Curie, 15 rue de l'Ecole de Médecine, 75006 Paris, France. Tel.: 33-1-42-34-69-18; Fax: 33-1-43-25-16-15; E-mail: jlebihan{at}bhdc.jussieu.fr.

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