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J Clin Med. 2016 Mar 23;5(4). pii: E39. doi: 10.3390/jcm5040039.

Osteopontin-A Master Regulator of Epithelial-Mesenchymal Transition.

Author information

1
Loyola University Medical Center, Department of Surgery, 2160 S First Ave, Maywood, IL 60153, USA. ankothari@lumc.edu.
2
Burn and Shock Trauma Institute, Loyola University Chicago, 2160 S First Ave, Maywood, IL 60153, USA. ankothari@lumc.edu.
3
Loyola University Medical Center, Department of Surgery, 2160 S First Ave, Maywood, IL 60153, USA. marffa@luc.edu.
4
Loyola University Medical Center, Department of Surgery, 2160 S First Ave, Maywood, IL 60153, USA. vchang@luc.edu.
5
Loyola University Medical Center, Department of Surgery, 2160 S First Ave, Maywood, IL 60153, USA. rblackwell@lumc.edu.
6
Division of Gastroenterology and Hepatology, Medical University of South Carolina, Charleston, South Carolina, USA. synw@musc.edu.
7
The Oncology Institute, Cardinal Bernardin Cancer Center, Loyola University Medical Center, Maywood, IL 60153, USA. jzhang@luc.edu.
8
Loyola University Medical Center, Department of Surgery, 2160 S First Ave, Maywood, IL 60153, USA. zhmi@luc.edu.
9
Loyola University Medical Center, Department of Surgery, 2160 S First Ave, Maywood, IL 60153, USA. paul.kuo@luhs.org.

Abstract

Osteopontin (OPN) plays an important functional role in both physiologic and pathologic states. OPN is implicated in the progression of fibrosis, cancer, and metastatic disease in several organ systems. The epithelial-mesenchymal transition (EMT), first described in embryology, is increasingly being recognized as a significant contributor to fibrotic phenotypes and tumor progression. Several well-established transcription factors regulate EMT and are conserved across tissue types and organ systems, including TWIST, zinc finger E-box-binding homeobox (ZEB), and SNAIL-family members. Recent literature points to an important relationship between OPN and EMT, implicating OPN as a key regulatory component of EMT programs. In this review, OPN's interplay with traditional EMT activators, both directly and indirectly, will be discussed. Also, OPN's ability to restructure the tissue and tumor microenvironment to indirectly modify EMT will be reviewed. Together, these diverse pathways demonstrate that OPN is able to modulate EMT and provide new targets for directing therapeutics.

KEYWORDS:

cancer-associated fibroblasts; epithelial-mesenchymal transition; fibrosis; osteopontin; tumor metastasis; tumor microenvironment

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