Cited by 2,804TGF-β signaling in diseasesCancer Cells and MetastasisDevelopmental Biology and Gene Regulation

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TGF-β-induced epithelial to mesenchymal transition

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Xu, Jian, Lamouille, Samy, Derynck, Rik·2009·Cell Research

DOI 10.1038/cr.2009.5PMC PMC4720263

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Abstract

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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Akhurst R . TGF-β signaling in epithelial-mesenchymal transition and invasion and metastasis. In: Derynck R, Miyazono K, eds. The TGF-beta family. Cold Spring Harbor Laboratory Press: New York 2007:939–964.

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Authors: Xu, J., Lamouille, S., & Derynck, R.
Affiliations: University of California, San Francisco (US)
Corresponding author: Derynck, Rik
ORCID: Xu, Jian
Lamouille, Samy
Derynck, Rik
Venue: Cell Research
Publisher: Springer Science and Business Media LLC
Published: 2009-01-20
Volume: 19
Issue: 2
Pages: 156-172
ISSN: 1001-0602 (ISSN-L)
1748-7838
DOI: 10.1038/cr.2009.5
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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TGF-β-induced epithelial to mesenchymal transition

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