Next Article in Journal / Special Issue
Signal Transduction Pathways of EMT Induced by TGF-β, SHH, and WNT and Their Crosstalks
Previous Article in Journal
Is there A Role for Alpha-Linolenic Acid in the Fetal Programming of Health?
Previous Article in Special Issue
New Insights into the Crossroads between EMT and Stemness in the Context of Cancer
Article Menu

Export Article

Open AccessReview
J. Clin. Med. 2016, 5(4), 39;

Osteopontin—A Master Regulator of Epithelial-Mesenchymal Transition

Loyola University Medical Center, Department of Surgery, 2160 S First Ave, Maywood, IL 60153, USA
Burn and Shock Trauma Institute, Loyola University Chicago, 2160 S First Ave, Maywood, IL 60153, USA
Division of Gastroenterology and Hepatology, Medical University of South Carolina, Charleston, South Carolina, USA
The Oncology Institute, Cardinal Bernardin Cancer Center, Loyola University Medical Center, Maywood, IL 60153, USA
Author to whom correspondence should be addressed.
Academic Editor: David T. Harris
Received: 21 December 2015 / Revised: 8 February 2016 / Accepted: 14 March 2016 / Published: 23 March 2016
(This article belongs to the Special Issue Epithelial-Mesenchymal Transition)
Full-Text   |   PDF [1311 KB, uploaded 23 March 2016]   |  


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. View Full-Text
Keywords: osteopontin; epithelial-mesenchymal transition; cancer-associated fibroblasts; tumor microenvironment; tumor metastasis; fibrosis osteopontin; epithelial-mesenchymal transition; cancer-associated fibroblasts; tumor microenvironment; tumor metastasis; fibrosis

Figure 1

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 (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Kothari, A.N.; Arffa, M.L.; Chang, V.; Blackwell, R.H.; Syn, W.-K.; Zhang, J.; Mi, Z.; Kuo, P.C. Osteopontin—A Master Regulator of Epithelial-Mesenchymal Transition. J. Clin. Med. 2016, 5, 39.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
J. Clin. Med. EISSN 2077-0383 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top