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

By Jonathan M. Lee, S. Dedhar, Raghu Kalluri, Erik W. Thompson. Journal of Cell Biology, 2006

2,061 citations recorded by the source corpus.

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).

Subfields: Genetics, Oncology

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Citations in the corpus

EMT, the cytoskeleton, and cancer cell invasion (2009, background): “Among the growth factors known to induce EMT are transforming growth factor β (TGFβ)[3], hepatocyte growth factor (HGF) [4], members of the epidermal growth factor (EGF) family [5], insulin-like growth factor (IGF)[6], and fibroblast growth factor (FGF)[7, 8].”
Colorectal Cancer Stem Cells Are Enriched in Xenogeneic Tumors Following Chemotherapy (2008, background): “In contrast, genes associated with differentiation and a mesenchymal phenotype [40, 41 ], such as Vimentin (VIM), were more highly expressed in NTG cells.”
Regulation of epithelial-mesenchymal transition through epigenetic and post-translational modifications (2016, background): “These junctions and interactions impede the movement of individual cells within the epithelial monolayer [3, 4].”
TGF-β-induced EMT: mechanisms and implications for fibrotic lung disease (2007, background): “Markers used to define the mesenchymal phenotype include vimentin, -SMA, fibroblast-specific protein-1 (FSP-1), desmin, (pro)-collagen, fibronectin, connective tissue growth factor (CTGF), N-cadherin, the transcription factors Snail and Slug, and expression of matrix metalloproteinases (MMPs) (52).”
Collective cell migration in morphogenesis, regeneration and cancer (2009, background): “This effect implicates E-cadherin as the dominant mediator of collective cell interactions, the loss of which may or may not be compensated for by other cell–cell adhesion pathway”
Notch signaling mediates hypoxia-induced tumor cell migration and invasion (2008, background): “EMT is accompanied by specific changes in gene expression, such as down-regulation of E-cadherin (6, 7).”
Epithelial-mesenchymal transition spectrum quantification and its efficacy in deciphering survival and drug responses of cancer patients (2014, positive): “First, we curated published EMT signatures (Subramanian et al , 2005; Lee et al , 2006; Carretero et al , 2010) and applied single-sample gene set enrichment analysis (ssGSEA) (Verhaak et al , 2013) to provide a gross assessment of the EMT phenotype of each cell line or tumour.”
Cisplatin Resistance: A Cellular Self-Defense Mechanism Resulting from Multiple Epigenetic and Genetic Changes (2012, background): “In the past several years, the epithelial to mesenchymal transition (EMT) and the Wnt (wingless gene) pathways have drawn increasing interest in the areas of developmental biology, cell differentiation, cell cycle, stem cells, cancer progression and treatment, and drug resistance (Lee et al., 2006; ”
Renal defects associated with improper polarization of the CRB and DLG polarity complexes in MALS-3 knockout mice (2007, neutral): “Alternatively, renal epithelia lacking MALS-3 may be increasingly susceptible to external cues, such as injury or infl ammation, which can trigger EMT (Kalluri and Neilson, 2003; J.M. Lee et al., 2006).”