TGF-β-induced epithelial to mesenchymal transition
By Jian Xu, Samy Lamouille, R. Derynck. Cell Research, 2009
2,369 citations recorded by the source corpus.
During development and in the context of different morphogenetic events, epithelial cells undergo a process called epithelial to mesenchymal transition or transdifferentiation (EMT). In this process, the cells lose their epithelial characteristics, including their polarity and specialized cell-cell contacts, and acquire a migratory behavior, allowing them to move away from their epithelial cell community and to integrate into surrounding tissue, even at remote locations. EMT illustrates the differentiation plasticity during development and is complemented by another process, called mesenchymal to epithelial transition (MET). While being an integral process during development, EMT is also recapitulated under pathological conditions, prominently in fibrosis and in invasion and metastasis of carcinomas. Accordingly, EMT is considered as an important step in tumor progression. TGF-β signaling has been shown to play an important role in EMT. In fact, adding TGF-β to epithelial cells in culture is a convenient way to induce EMT in various epithelial cells. Although much less characterized, epithelial plasticity can also be regulated by TGF-β-related bone morphogenetic proteins (BMPs), and BMPs have been shown to induce EMT or MET depending on the developmental context. In this review, we will discuss the induction of EMT in response to TGF-β, and focus on the underlying signaling and transcription mechanisms.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/a7af32cca65b19a1e7528b114bc3ce6ea6961812
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In Molecular Biology
- Hans Clevers
- Nikolaos G. Frangogiannis
- M. van de Wetering
- H. Gehart
- Alexey I. Nesvizhskii
- R. Vries
- Meritxell Huch
- Steven A. Carr
In Oncology
Citations in the corpus
- Epithelial-Mesenchymal Transition in Cancer: A Historical Overview (2020, background): “It has been demonstrated that transforming growth factor beta (TGF-β)/Smads pathway is the strongest EMT inducer by the upregulation of EMT-related transcription factors [23].”
- Long-Term Culture of Genome-Stable Bipotent Stem Cells from Adult Human Liver (2015, positive): “Tgf-b signaling induces growth arrest and epithelial-to-mesenchymal transition (Xu et al., 2009).”
- Proteogenomic characterization reveals therapeutic vulnerabilities in lung adenocarcinoma (2020, background): “SMADs 2 and 4 are key elements in the transcriptional regulation of epithelial-mesenchymal transition (EMT) induced by transforming growth factor b (TGF-b) signaling (Xu et al., 2009).”
- Chronic Inflammation and Cytokines in the Tumor Microenvironment (2014, background): “The immune response comprises a series of events triggered in response to recognition of pathogens or tissue damage, involving cells and soluble mediators, such as cytokines of”
- TGF-β signaling in fibrosis (2011, background): “In addition to mesenchymal cells, myofibroblasts may derive from epithelial origin in a process termed epithelial–mesenchymal transition (EMT) (Krenning et al. 2010).”
- The extracellular matrix at a glance (2010, background): “In some instances, the release of transforming growth factor (TGF-) by tension and MMPs induces EMT of the resident epithelium (Schultz and Wysocki, 2009; Wipff et al., 2007; Xu et al., 2009).”