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BioMed Research International
Volume 2017, Article ID 6138145, 18 pages
Review Article

The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression

Department of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary

Correspondence should be addressed to János Kappelmayer; uh.bedinu.dem@reyamleppak

Received 2 February 2017; Revised 12 April 2017; Accepted 23 April 2017; Published 7 June 2017

Academic Editor: Marlien Pieters

Copyright © 2017 János Kappelmayer and Béla Nagy Jr. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Cellular interaction is inevitable in the pathomechanism of human disease. Formation of heterotypic cellular aggregates, between distinct cells of hematopoietic and nonhematopoietic origin, may be involved in events leading to inflammation and the complex process of cancer progression. Among adhesion receptors, the family of selectins with their ligands have been considered as one of the major contributors to cell-cell interactions. Consequently, the inhibition of the interplay between selectins and their ligands may have potential therapeutic benefits. In this review, we focus on the current evidence on the selectins as crucial modulators of inflammatory, thrombotic, and malignant disorders. Knowing that there is promiscuity in selectin binding, we outline the importance of a key protein that serves as a ligand for all selectins. This dimeric mucin, the P-selectin glycoprotein ligand 1 (PSGL-1), has emerged as a major player in inflammation, thrombus, and cancer development. We discuss the interaction of PSGL-1 with various selectins in physiological and pathological processes with particular emphasis on mechanisms that lead to severe disease.