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Integrins and E‐cadherin cooperate with IGF‐I to induce migration of epithelial colonic cells
Author(s) -
André Frédéric,
Rigot Véronique,
Thimonier Jean,
Montixi Christine,
Parat Fabrice,
Pommier Gilbert,
Marvaldi Jacques,
Luis José
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19991112)83:4<497::aid-ijc11>3.0.co;2-d
Subject(s) - integrin , microbiology and biotechnology , cadherin , cell adhesion molecule , catenin , tyrosine phosphorylation , cell migration , cell adhesion , biology , tyrosine kinase , phosphorylation , cell , signal transduction , biochemistry , wnt signaling pathway
Although the detailed mechanisms of cell migration remain largely unknown, it is now clear that growth factors and cell adhesion molecules are crucial for this process. We have shown that type I insulin‐like growth factor (IGF‐I) promotes migration of human colonic tumour cells. Since morphological analysis suggested an involvement of adhesion molecules, we have now examined the role of integrins (cell‐matrix adhesion molecules) and E‐cadherin/catenins complex (cell‐cell adhesion molecules) in the IGF‐I‐induced migration. Using a monolayer wounding assay, we have determined that, except for α2β1, all of the integrins expressed in HT29‐D4 cells are involved in the induced cell migration. Immunofluorescence studies revealed that upon IGF‐I stimulation the integrins reorganized at the leading edge of migrating cells. We also demonstrate that E‐cadherin is involved in cell migration. A rapid tyrosine phosphorylation of E‐cadherin and β‐catenin was detected upon IGF‐I stimulation. Tyrosine phosphorylation was associated with reduced membranous expression of E‐cadherin and promotion of cell motility, suggesting a regulation of the E‐cadherin/catenins complex. This effect can be reversed by incubating cells with tyrosine kinase inhibitors. Taken together, our results suggest that IGF‐I promotes colonic cell migration through reorganization of integrin receptors and through modulation of E‐cadherin/catenins complex function. Int. J. Cancer 83: 497–505, 1999. © 1999 Wiley‐Liss, Inc.