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Published 27 March 2006. doi:10.1083/jcb.200601018
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 172, Number 7, 973-981
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Mini-Review

The epithelial–mesenchymal transition: new insights in signaling, development, and disease



Jonathan M. Lee1, Shoukat Dedhar2,3, Raghu Kalluri4,5,6, and Erik W. Thompson7,8

1 Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario K1N 6N5, Canada
2 Department of Biochemistry, University of British Columbia, Vancouver, British Columbia V57 1L3, Canada
3 British Columbia Cancer and Research Centre at the British Columbia Cancer Agency, Vancouver, British Columbia V57 1L3, Canada
4 Department of Medicine, Center for Matrix Biology, Beth Israel Deaconess Medical Center and 5 Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02215
6 Harvard–Massachusetts Institute of Technology Division of Health Sciences and Technology, Cambridge, MA 02139
7 Department of Surgery, University of Melbourne, St. Vincent's Hospital, Fitzroy, 3065, Australia
8 St. Vincent's Institute of Medical Research, Fitzroy, 3065, Australia

Correspondence to Shoukat Dedhar: sdedhar{at}interchange.ubc.ca


Abstract

The conversion of an epithelial cell to a mesenchymal cell is critical to metazoan embryogenesis and a defining structural feature of organ development. Current interest in this process, which is described as an epithelial–mesenchymal transition (EMT), stems from its developmental importance and its involvement in several adult pathologies. Interest and research in EMT are currently at a high level, as seen by the attendance at the recent EMT meeting in Vancouver, Canada (October 1–3, 2005). The meeting, which was hosted by The EMT International Association, was the second international EMT meeting, the first being held in Port Douglas, Queensland, Australia in October 2003. The EMT International Association was formed in 2002 to provide an international body for those interested in EMT and the reverse process, mesenchymal–epithelial transition, and, most importantly, to bring together those working on EMT in development, cancer, fibrosis, and pathology. These themes continued during the recent meeting in Vancouver.

Discussion at the Vancouver meeting spanned several areas of research, including signaling pathway activation of EMT and the transcription factors and gene targets involved. Also covered in detail was the basic cell biology of EMT and its role in cancer and fibrosis, as well as the identification of new markers to facilitate the observation of EMT in vivo. This is particularly important because the potential contribution of EMT during neoplasia is the subject of vigorous scientific debate (Tarin, D., E.W. Thompson, and D.F. Newgreen. 2005. Cancer Res. 65:5996–6000; Thompson, E.W., D.F. Newgreen, and D. Tarin. 2005. Cancer Res. 65:5991–5995).

Abbreviations used in this paper: BMP7, bone-morphogenic protein 7; EGFR, EGF receptor; EMT, epithelial–mesenchymal transition; ER, estrogen receptor; FSP1, fibroblast-specific protein 1; GSK, glycogen synthase kinase; ILK, integrin-linked kinase; MET, mesenchymal–epithelial transition; MMP, matrix metalloproteinase; OSE, ovarian surface epithelium; PARP-1, poly-ADP-ribose polymerase 1; ROS, reactive oxygen species; siRNA, small interfering RNA.


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