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PMID: 19903090 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Review

Epithelial-mesenchymal transition: from molecular mechanisms, redox regulation to implications in human health and disease.

Antioxidants & redox signaling ·Vol. 12 ·No. 12 ·2010-06-15 ·Pages 1383-430

Cannito S, Novo E, di Bonzo LV, Busletta C, Colombatto S, Parola M

Abstract

Epithelial to mesenchymal transition (EMT) is a fundamental process, paradigmatic of the concept of cell plasticity, that leads epithelial cells to lose their polarization and specialized junctional structures, to undergo cytoskeleton reorganization, and to acquire morphological and functional features of mesenchymal-like cells. Although EMT has been originally described in embryonic development, where cell migration and tissue remodeling have a primary role in regulating morphogenesis in multicellular organisms, recent literature has provided evidence suggesting that the EMT process is a more general biological process that is also involved in several pathophysiological conditions, including cancer progression and organ fibrosis. This review offers first a comprehensive introduction to describe major relevant features of EMT, followed by sections dedicated on those signaling mechanisms that are known to regulate or affect the process, including the recently proposed role for oxidative stress and reactive oxygen species (ROS). Current literature data involving EMT in both physiological conditions (i.e., embryogenesis) and major human diseases are then critically analyzed, with a special final focus on the emerging role of hypoxia as a relevant independent condition able to trigger EMT.

MeSH Terms
Cell Dedifferentiation/physiology Cell Hypoxia Cell Polarity Cytoskeleton/ultrastructure Embryonic Development/physiology Endothelial Cells/cytology Epithelial Cells/cytology Extracellular Matrix Proteins/physiology Fibrosis/pathology Gene Expression Regulation Humans Mesoderm/cytology MicroRNAs/physiology Neoplasms/pathology Oxidation-Reduction Oxidative Stress Reactive Oxygen Species Signal Transduction/physiology Transcription Factors/physiology Wound Healing/physiology
Chemicals
Extracellular Matrix Proteins MicroRNAs Reactive Oxygen Species Transcription Factors
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Cannito Stefania
Department of Experimental Medicine and Oncology and Interuniversity Center for Hepatic Pathophysiology, University of Turin, Turin, Italy.
Novo Erica
di Bonzo Lorenzo Valfrè
Busletta Chiara
Colombatto Sebastiano
Parola Maurizio
Article Info
Journal
Antioxidants & redox signaling
Abbr.
Antioxid Redox Signal
ISSN
1557-7716
Published
2010-06-15
Pages
1383-430
Language
English
Region
United States
NLM ID
100888899
Subset
IM
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