Molecular mechanisms of epithelial–mesenchymal transition
Open accessAbstract
The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT), is integral in development, wound healing and stem cell behaviour, and contributes pathologically to fibrosis and cancer progression. This switch in cell differentiation and behaviour is mediated by key transcription factors, including SNAIL, zinc-finger E-box-binding (ZEB) and basic helix-loop-helix transcription factors, the functions of which are finely regulated at the transcriptional, translational and post-translational levels. The reprogramming of gene expression during EMT, as well as non-transcriptional changes, are initiated and controlled by signalling pathways that respond to extracellular cues. Among these, transforming growth factor-β (TGFβ) family signalling has a predominant role; however, the convergence of signalling pathways is essential for EMT.
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Activation of the Wnt/β-catenin/EMT axis accounts for the invasive characteristics observed, linking this signaling cascade to ccRCC metastasis.
“Likewise, the activation of the Wnt/β-catenin/EMT axis accounts for the invasive characteristics we observed, linking this signaling cascade to ccRCC metastasis [34, 35].”
From PPP1R18-mediated activation of Wnt/β-catenin and EMT is dependent on ERK signaling in clear cell renal cell carcinoma (2026) · cites this paper as [34]
The section “Other extracellular signals regulate EMT” states that WNT signalling promotes EMT associated with cancer progression and that β-catenin-mediated gene expression increases at the invasive front of colorectal tumours (page unavailable). It does not address the citing authors’ observed invasive characteristics or establish this pathway as an explanation for ccRCC metastasis. (LLM, conf=0.86)
Experimental — accuracy not yet measuredEMT is a critical biological process by which tumor cells acquire motility and invasiveness, is a hallmark of metastasis, and is frequently regulated by Wnt/β-catenin signaling.
“EMT, a critical biological process by which tumor cells acquire motility and invasiveness, is a hallmark of metastasis and is frequently regulated by Wnt/β-catenin signaling [33–35].”
From PPP1R18-mediated activation of Wnt/β-catenin and EMT is dependent on ERK signaling in clear cell renal cell carcinoma (2026) · cites this paper as [34]
During fibroblast-to-myofibroblast transition, complex mechanochemical signaling is activated involving profibrotic secreted factors TGFβ and Wnt and ECM-degrading enzymes and intracellular effectors required for stress fiber contractility.
“During fibroblast-to-myofibroblast transition, a complex mechanochemical signaling is activated involving profibrotic secreted factors such as TGFβ and Wnt and ECM-degrading enzymes and intracellular effectors required for stress fiber contractility [127,131].”
From Cellular and Molecular Mechanisms in the Pathogenesis of Classical, Vascular, and Hypermobile Ehlers‒Danlos Syndromes (2019) · cites this paper as [127]
TGF-β-driven EMT mainly depends on TβRI and Smad3/4 turning on master EMT transcription factors such as Snail1, Snail2/Slug, ZEB1, and ZEB2; these factors then work with Smad3/4 to suppress epithelial genes and induce mesenchymal ones.
“The ability of TGF-β to promote epithelial plasticity and EMT results primarily from activation of TβRI, enabling Smad3/4-mediated activation of genes that encode master EMT transcription factors, such as Snail1 and Snail2/Slug, and ZEB1 and ZEB2. These in turn cooperate with Smad3/4 complexes to repress epithelial and activate mesenchymal genes128.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [128]
Treatment of rats, mice, and pigs with GHK effectively activates systemic healing throughout the animal.
“The treatment of rats, mice, and pigs with GHK was shown to effectively activate systemic healing throughout the animal.”
From GHK and DNA: Resetting the human genome to health (2014) · cites this paper as [45]
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“EMT is characterized by reduced intercellular adhesion, loss of epithelial markers (such as E-cadherin), and acquisition *Correspondence: langchen@whu.edu.cn; dguo@whu.edu.cn; ghsunlab@whu.edu.cn 1 School of Basic Medical Sciences, Wuhan University, Wuhan 430072, People’s Republic of China Full list of author informat…”
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“Likewise, the activation of the Wnt/β-catenin/EMT axis accounts for the invasive characteristics we observed, linking this signaling cascade to ccRCC metastasis [34, 35].”
- Authors
- Lamouille, S., Xu, J., & Derynck, R.
- Affiliations
- University of California, San Francisco (US)
- University of Southern California (US)
- Corresponding author
- Derynck, Rik
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2014-02-21
- Volume
- 15
- Issue
- 3
- Pages
- 178-196
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- PMC
- PMC4240281
- OpenAlex
- W1964847767
- Cited by
- 8,091
- References
- 270
- Citations by year
- 2026: 383 · 2025: 515 · 2024: 687 · 2023: 709 · 2022: 812 · 2021: 905 · 2020: 886 · 2019: 759 · 2018: 730 · 2017: 690 · 2016: 559 · 2015: 336 · 2014: 115 · 2013: 1
- FWCI
- 64.30
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Cancer Institute (R01CA136690)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- epithelial-mesenchymal transition, transcription factors, snails, ZEB, bHLH transcription factors, transforming growth factor-beta signalling, transdifferentiation, fibrosis, tumor progression, gene expression reprogramming, post-translational regulation
- MeSH terms
- Cell Movement, Cytoskeleton, Humans, Models, Biological, RNA, Transcription Factors, Signal Transduction, Gene Expression Regulation, Developmental, Epithelial-Mesenchymal Transition
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