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Mediators of Inflammation
Volume 2017, Article ID 4049098, 22 pages
https://doi.org/10.1155/2017/4049098
Review Article

Osteopontin at the Crossroads of Inflammation and Tumor Progression

1Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy
2Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), University of Eastern Piedmont, Novara, Italy
3SCDU Anestesia e Rianimazione, Azienda Ospedaliero-Universitaria Maggiore della Carità, Novara, Italy
4Department of Translational Medicine, Nephrology and Kidney Transplant Unit, University of Eastern Piedmont, Novara, Italy
5Department of Health Sciences, University of Eastern Piedmont, Novara, Italy
6Department of Surgery, University of Eastern Piedmont, Novara, Italy
7Anestesia e Rianimazione, Università “Magna Graecia” di Catanzaro, Catanzaro, Italy

Correspondence should be addressed to Anna Aspesi; ti.opuinu.dem@isepsa.anna

Received 14 April 2017; Accepted 4 June 2017; Published 9 July 2017

Academic Editor: Rajesh Singh

Copyright © 2017 Luigi Mario Castello et al. 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.

Abstract

Complex interactions between tumor and host cells regulate systemic tumor dissemination, a process that begins early at the primary tumor site and goes on until tumor cells detach themselves from the tumor mass and start migrating into the blood or lymphatic vessels. Metastatic cells colonize the target organs and are capable of surviving and growing at distant sites. In this context, osteopontin (OPN) appears to be a key determinant of the crosstalk between cancer cells and the host microenvironment, which in turn modulates immune evasion. OPN is overexpressed in several human carcinomas and has been implicated in inflammation, tumor progression, and metastasis. Thus, it represents one of the most attracting targets for cancer therapy. Within the tumor mass, OPN is secreted in various forms either by the tumor itself or by stroma cells, and it can exert either pro- or antitumorigenic effects according to the cell type and tumor microenvironment. Thus, targeting OPN for therapeutic purposes needs to take into account the heterogeneous functions of the multiple OPN forms with regard to cancer formation and progression. In this review, we will describe the role of systemic, tumor-derived, and stroma-derived OPN, highlighting its pivotal role at the crossroads of inflammation and tumor progression.