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Research article

Intestinal HT-29 cells with dysfunction of E-cadherin show increased pp60src activity and tyrosine phosphorylation of p120-catenin

Anouchka SKOUDY, Maria del Mont LLOSAS, Antonio GARCÍA de HERREROS
Biochemical Journal Jul 01, 1996, 317 (1) 279-284; DOI: 10.1042/bj3170279
Anouchka SKOUDY
Unitat de Biologia Cel.lular i Molecular, Institut Municipal d'Investigació Mèdica, Universitat Autònoma de Barcelona, C/ Dr. Aiguader, 80, 08003 Barcelona, Spain
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Maria del Mont LLOSAS
Unitat de Biologia Cel.lular i Molecular, Institut Municipal d'Investigació Mèdica, Universitat Autònoma de Barcelona, C/ Dr. Aiguader, 80, 08003 Barcelona, Spain
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Antonio GARCÍA de HERREROS
Unitat de Biologia Cel.lular i Molecular, Institut Municipal d'Investigació Mèdica, Universitat Autònoma de Barcelona, C/ Dr. Aiguader, 80, 08003 Barcelona, Spain
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Abstract

1. HT-29 M6 cells are a subpopulation of HT-29 cells that, contrarily to the parental cells, establish tight cell contacts and differentiate. Cell-to-cell contacts in HT-29 M6 cells are also regulated by protein kinase C; addition of the phorbol ester phorbol 12-myristate 13-acetate (PMA) decreases the homotypic contacts of these cells. We show here that HT-29 cells or HT-29 M6 cells treated with PMA contain lower levels of functional E-cadherin, determined by analysing the association of this protein with the cytoskeleton. No significant differences in the localization of α-, β-, or p120-catenins were detected under the three different conditions. 2. Dysfunction of E-cadherin can be reversed by incubation of HT-29 cells with the tyrosine kinase inhibitor herbimycin A. On the other hand an augmentation of c-src activity in HT-29 cells or HT-29 M6 cells treated with PMA was observed with respect to control HT-29 M6 cells. The phosphorylation status of catenins was also investigated; in HT-29 or in HT-29 M6 cells treated with PMA, dysfunction of E-cadherin was accompanied by an increased phosphorylation of p120-catenin and by an elevated association of this protein to E-cadherin. These results suggest a role for pp60src and the pp60src substrate p120-catenin in the control of E-cadherin function in HT-29 cells.

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July 1996

Volume: 317 Issue: 1

Biochemical Journal: 317 (1)
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Intestinal HT-29 cells with dysfunction of E-cadherin show increased pp60src activity and tyrosine phosphorylation of p120-catenin
Anouchka SKOUDY, Maria del Mont LLOSAS, Antonio GARCÍA de HERREROS
Biochemical Journal Jul 1996, 317 (1) 279-284; DOI: 10.1042/bj3170279
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Intestinal HT-29 cells with dysfunction of E-cadherin show increased pp60src activity and tyrosine phosphorylation of p120-catenin
Anouchka SKOUDY, Maria del Mont LLOSAS, Antonio GARCÍA de HERREROS
Biochemical Journal Jul 1996, 317 (1) 279-284; DOI: 10.1042/bj3170279

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