1. ¹Department of Medicine, Vanderbilt School of Medicine, Nashville, TN, USA
2. ²Department of Cancer Biology, Vanderbilt School of Medicine, Nashville, TN, USA
3. ³Molecular Physiology and Biophysics, Vanderbilt School of Medicine, Nashville, TN, USA

Correspondence: Volker H. Haase, Department of Medicine, Vanderbilt University Medical Center, C-3119A, MCN, 1161 21stAvenue, Nashville, TN 37232, USA. E-mail: volker.haase@vanderbilt.edu

Received 20 January 2009; Revised 10 March 2009; Accepted 1 April 2009; Published online 17 June 2009.

Abstract

Epithelial-to-mesenchymal transition (EMT) is a developmentally vital, molecularly complex cellular process by which epithelial cells lose apico–basal polarity and cell–cell contact, become motile, and acquire mesenchymal characteristics. Under pathophysiological conditions EMT has a central role in cancer progression and metastasis, and has been associated with fibrotic disorders. Microenvironmental changes such as alterations in oxygen levels and activation of hypoxic signaling through hypoxia-inducible factor (HIF) are emerging as important triggers and modulators of EMT. Recent insights into potential molecular mechanisms underlying oxygen-dependent regulation of this process and their relevance to disease are discussed.