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Int J Oncol. 2004 Nov;25(5):1459-64.

Transactivation of E-cadherin is not involved in the activity of EGF receptor in colorectal carcinoma cells.

Author information

1
Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Flemingovo nám. 2, 166 37 Prague 6, Czech Republic. sova@img.cas.cz

Abstract

In epithelial cells, the cell surface glycoprotein E-cadherin is a key molecule in the establishment of cell-cell adhesion. In addition to its contribution to cell adhesion, E-cadherin was found to induce ligand-independent activation of the EGF receptor (EGFR), likely as a result of their co-clustering. As it has also been reported that ligand activation of the overexpressed EGFRs disturb E-cadherin-mediated cell-cell adhesion, we analyzed E-cadherin-EGFR interactions and their consequences in A431 cells and in two colorectal cancer cell lines using immunoblotting and analyzes of several protein kinase activities. Activation of the PI3-K/Akt/GSK-3 signaling pathway upon EGF treatment that we observed in the analyzed cells indicates that EGFRs are functional even in the colorectal cancer cells containing a low density of EGFRs. The transactivation of EGFR by E-cadherin did not occur either in the colorectal cancer cells tested or in A431 cells containing a high density of both EGFRs and E-cadherin on their surface. This observation suggests that high amounts of both molecules on the surface of tumour cells did not predetermine ligand-independent activation of EGFRs.

PMID:
15492839
[Indexed for MEDLINE]

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