Fibrinogen mediates bladder cancer cell migration in an ICAM-1-dependent pathway

• Published in: Thrombosis and haemostasis Vol. 89; no. 6; p. 1089
• Main Authors: Roche, Yann, Pasquier, Dominique, Rambeaud, Jean-Jacques, Seigneurin, Daniel, Duperray, Alain
• Format: Journal Article
• Language: English
• Published: Germany 01.06.2003
• Subjects: Cell Communication; Cell Line, Tumor; Cell Movement; Endothelium, Vascular - cytology; Fibrinogen - metabolism; Fibrinogen - physiology; Focal Adhesions; Humans; Intercellular Adhesion Molecule-1 - metabolism; Neoplasm Invasiveness - pathology; Neoplasm Metastasis - pathology; Protein Binding; rhoA GTP-Binding Protein - metabolism; Umbilical Veins - cytology; Urinary Bladder Neoplasms - pathology
• ISSN: 0340-6245
• DOI: 10.1055/s-0037-1613412

Fibrinogen (fg), present in tumor matrices, has been demonstrated to be determinant in metastatic potential. We have recently shown that fg/ICAM-1 interactions are involved in leukocyte migration across endothelial cell monolayers. Using bladder transitional cell carcinoma as a model, we will show in this study that bladder high grade tumor cell lines express ICAM-1, and that this expression induces an fg-mediated migration. This phenomenon was dependent on ICAM-1/fg interaction as well as RhoA activity. ICAM-1 was concentrated in focal adhesion plaques when tumor cells were allowed to adhere on immobilized fg, suggesting a role in cell migration. The addition of fg induced a 3- to 6-fold enhancement of bladder tumor cell migration through HUVEC monolayers. This process was inhibited by an anti-ICAM-1 antibody blocking fg binding, demonstrating that ICAM-1/fg interaction was involved in the extravasation process. Finally, immunohistological studies revealed that the expression of ICAM-1 was closely associated with an infiltrative histological phenotype.