Summary

Fibrinogen (fg), present in tumor matrices, has been demonstratedto be determinant in metastatic potential. We haverecently shown that fg/ICAM-1 interactions are involved in leukocytemigration across endothelial cell monolayers. Usingbladder transitional cell carcinoma as a model, we will show inthis study that bladder high grade tumor cell lines expressICAM-1, and that this expression induces an fg-mediated migration.This phenomenon was dependent on ICAM-1/fg interactionas well as RhoA activity. ICAM-1 was concentrated in focal adhesion plaques when tumor cells were allowed to adhere onimmobilized fg, suggesting a role in cell migration.The additionof fg induced a 3- to 6-fold enhancement of bladder tumor cellmigration through HUVEC monolayers.This process was inhibitedby an anti-ICAM-1 antibody blocking fg binding, demonstratingthat ICAM-1/fg interaction was involved in the extravasationprocess. Finally, immunohistological studies revealedthat the expression of ICAM-1 was closely associated with aninfiltrative histological phenotype.