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TGF-β-induced epithelial to mesenchymal transition
Open accessAbstract
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-beta signaling has been shown to play an important role in EMT. In fact, adding TGF-beta 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-beta-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-beta, and focus on the underlying signaling and transcription mechanisms.
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“EMT plays an important role in cancer progression and is induced by TGFβ [23].”
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“Adding TGF-β induces EMT in diverse epithelial cell cultures via the SMAD signaling pathway (56).”
From Tumor-Induced Inflammatory Cytokines and the Emerging Diagnostic Devices for Cancer Detection and Prognosis (2021) · cites this paper as [56]
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Metadata
- Authors
- Xu, J., Lamouille, S., & Derynck, R.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- Derynck, Rik
- Venue
- Cell Research
- Published
- 2009-01-20
- Volume
- 19
- Issue
- 2
- Pages
- 156-172
- ISSN
- 1001-0602 (ISSN-L)
- 1748-7838
- PMC
- PMC4720263
- OpenAlex
- W1760215417
- Cited by
- 2,804
- References
- 167
- Citations by year
- 2026: 123 · 2025: 178 · 2024: 186 · 2023: 207 · 2022: 252 · 2021: 242 · 2020: 220 · 2019: 174 · 2018: 190 · 2017: 197 · 2016: 162 · 2015: 148 · 2014: 149 · 2013: 111 · 2012: 95
- FWCI
- 6.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01HL060231)
- National Center for Research Resources (P41RR001614)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- epithelial-mesenchymal transition, TGF-beta signaling, mesenchymal-epithelial transition, epithelial plasticity, bone morphogenetic proteins, cell migration, tumor progression, fibrosis, tumor invasion and metastasis, cell polarity, transcriptional regulation
- MeSH terms
- Epithelial Cells, Mesoderm, Transcription Factors, Signal Transduction, Transforming Growth Factor beta, Bone Morphogenetic Proteins, Smad Proteins, Cell Transdifferentiation
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