Associate Professor of Medicine, Harvard Medical School.
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Mechanisms of metastasis: Epithelial-to-mesenchymal transition and contribution of tumor microenvironment
Article first published online: 22 JAN 2007
DOI: 10.1002/jcb.21215
Copyright © 2007 Wiley-Liss, Inc.
Additional Information
How to Cite
Tse, J. C. and Kalluri, R. (2007), Mechanisms of metastasis: Epithelial-to-mesenchymal transition and contribution of tumor microenvironment. J. Cell. Biochem., 101: 816–829. doi: 10.1002/jcb.21215
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Associate Professor of Medicine, Harvard Medical School.
Publication History
- Issue published online: 13 JUN 2007
- Article first published online: 22 JAN 2007
- Manuscript Accepted: 30 OCT 2006
- Manuscript Received: 25 OCT 2006
Funded by
- BIDMC
- Abstract
- Article
- References
- Cited By
Keywords:
- cancer;
- metastasis;
- epithelial to mesenchymal transition;
- EMT;
- mesenchymal to epithelial transition;
- MET;
- tumor microenvironment;
- extracellular matrix
Abstract
Every year about 500,000 people in the United States die as a result of cancer. Among them, 90% exhibit systemic disease with metastasis. Considering this high rate of incidence and mortality, it is critical to understand the mechanisms behind metastasis and identify new targets for therapy. In recent years, two broad mechanisms for metastasis have received significant attention: epithelial-to-mesenchymal transition (EMT) and tumor microenvironment interactions. EMT is believed to be a major mechanism by which cancer cells become migratory and invasive. Various cancer cells—both in vivo and in vitro—demonstrate features of epithelial-to-mesenchymal-like transition. In addition, many steps of metastasis are influenced by host contributions from the tumor microenvironment, which help determine the course and severity of metastasis. Here we evaluate the diverse mechanisms of EMT and tumor microenvironment interactions in the progression of cancer, and construct a rational argument for targeting these pathways to control metastasis. J. Cell. Biochem. 101: 816–829, 2007. © 2007 Wiley-Liss, Inc.