부산대학교 도서관

The mechanisms by which growth factors cooperate with cell adhesion molecules to modulate epithelial cell motility remain poorly understood. Here, we investigated the role of the E-cadherin/catenin complex in insulin-like growth factor (IGF-I)-dependent cell migration and invasion. We used variants of the HCT-8 colon cancer family that differ in their expression of aE-catenin, an intracellular molecule that links the E-cadherin/catenin complex to the actin cytoskeleton. Migration was determined using a monolayer wound model and cell invasion by the penetration of the cells into type-I collagen gels. We showed that a-catenin-deficient cells were not able to migrate in cohort upon IGF-I stimulation. Transfection of these cells with a-catenin isoforms (aN- or aT-catenin) restored migratory response IGF-I. These results suggest that a-catenins are involved in the signal issued from the E-cadherin/catenin complex to regulate IGF-I-stimulated migration. In contrast, IGF-I promoted invasion of both a-catenin-deficient and a-catenin-expressing cells, indicating that a-catenin did not participate in the regulation of IGF-I-induced invasion. Inhibition of E-cadherin function by treatment with MB-2 monoclonal antibodies inhibited both IGF-I-dependent cell migration and invasion. Taken together, our results indicate that functional a-catenin is essential for migration but not for invasion, while E-cadherin is involved in both phenomena.Oncogene (2004) 23, 1177-1186. doi:10.1038/sj.onc.1207238 [ABSTRACT FROM AUTHOR]