help button home button Am J Pathol R & D Systems
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Boccellino, M.
Right arrow Articles by Quagliuolo, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Boccellino, M.
Right arrow Articles by Quagliuolo, L.
(American Journal of Pathology. 2005;166:1515-1522.)
© 2005 American Society for Investigative Pathology

Platelet-Activating Factor Regulates Cadherin-Catenin Adhesion System Expression and ß-Catenin Phosphorylation during Kaposi’s Sarcoma Cell Motility

Mariarosaria Boccellino*, Giovanni Camussi{dagger}, Alfonso Giovane*, Luigi Ferro*, Vincenzo Calderaro{ddagger}, Ciro Balestrieri* and Lucio Quagliuolo*

From the Dipartimento di Biochimica e Biofisica* and the Istituto di Medicina Interna e Nefrologia, Facoltà di Medicina e Chirurgia,{ddagger} Seconda Università degli Studi di Napoli; and the Dipartimento di Medicina Interna,{dagger} Università di Torino, Torino, Italy

In the present study, we evaluated whether motility of Kaposi’s sarcoma (KS) cells induced by platelet-activating factor (PAF) is dependent on the regulation of adherens junctions components. The results obtained indicate that PAF dose and time dependently reduced the endogenous expression of the main components of the adherens junctions: VE-cadherin, {alpha}-catenin, and ß-catenin. In addition, PAF initiated events that directly or indirectly up-regulated both the tyrosine and serine/threonine phosphorylation pathways, and both types of phosphorylation of ß-catenin were involved in the motility of KS cells. This motility was abrogated by addition of the tyrosine kinase inhibitor genistein, suggesting that this phosphorylation is an important signal responsible for breaking down the adherens junctions and diminishing the ability of neighboring cells to interact. Furthermore, immunofluorescence analysis showed that ß-catenin and VE-cadherin staining changed from a uniform distribution along the membrane of controls to a diffuse pattern with gap formation in PAF-treated KS cells. In conclusion, the data presented here indicate that PAF induces tumor cell motility by altering cell-cell adhesion through ß-catenin phosphorylation.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by the American Society for Investigative Pathology.