The basics of epithelial-mesenchymal transition
Open accessAbstract
The origins of the mesenchymal cells participating in tissue repair and pathological processes, notably tissue fibrosis, tumor invasiveness, and metastasis, are poorly understood. However, emerging evidence suggests that epithelial-mesenchymal transitions (EMTs) represent one important source of these cells. As we discuss here, processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias. The identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes and possible therapeutic interventions.
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Epithelial-to-mesenchymal transition (EMT) plays a critical role in driving phenotypic diversity in solid tumors by suppressing epithelial markers such as E-cadherin and upregulating mesenchymal markers like vimentin and N-cadherin.
“In addition to these models, EMT plays a critical role in driving phenotypic diversity in solid tumors. Through EMT, epithelial cancer cells undergo a dynamic reprogramming process that suppresses epithelial markers, such as E-cadherin, while upregulating mesenchymal markers, like vimentin and N-cadherin [130,131].”
From Modeling Tumor Microenvironment Complexity In Vitro: Spheroids as Physiologically Relevant Tumor Models and Strategies for Their Analysis (2025) · cites this paper as [131]
The Type 3 EMT section links EMT in carcinoma cells to varied epithelial and mesenchymal traits, loss of E-cadherin, and expression of vimentin. It does not support N-cadherin upregulation in cancer EMT; the Type 1 EMT section instead says N-cadherin must be repressed during neural crest EMT. The paper also describes EMT as a proposed critical mechanism in cancer, rather than an established driver of phenotypic diversity across solid tumors. (LLM, conf=0.87)
Experimental — accuracy not yet measuredEMT imparts enhanced migratory and invasive capacity, survival advantage under stress, and increased resistance to apoptotic stimuli.
“This transition imparts enhanced migratory and invasive capacity, survival advantage under stress, and increased resistance to apoptotic stimuli [39,131,132,133].”
From Modeling Tumor Microenvironment Complexity In Vitro: Spheroids as Physiologically Relevant Tumor Models and Strategies for Their Analysis (2025) · cites this paper as [131]
The section “What is epithelial-mesenchymal transition?” (page unavailable) explicitly lists enhanced migratory capacity, invasiveness, and elevated resistance to apoptosis as EMT-associated traits. The Type 3 EMT section suggests that cancer-cell EMT may prevent oncogene-induced senescence, but the copy does not establish the broader claim of a survival advantage under stress. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTGF-β influences CAF expression of cytokines and chemokines that act on cancer, endothelial and/or immune cells, such as HGF, VEGF, IL-6, IL-8, MCP1, PGE2 and CXCL12.
“Finally, TGF-β influences CAF expression of cytokines and chemokines that act on cancer, endothelial and/or immune cells, such as HGF245, VEGF, IL-6, IL-8, MCP1, PGE2 and CXCL12229,257–262.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [258]
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References 139 · Cited by 10,196
- Authors
- Kalluri, R., & Weinberg, R. A.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Whitehead Institute for Biomedical Research (US)
- Corresponding author
- Kalluri, Raghu
- Venue
- Journal of Clinical Investigation
- Published
- 2009-06-01
- Volume
- 119
- Issue
- 6
- Pages
- 1420-1428
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC2689101
- OpenAlex
- W2154589460
- Cited by
- 10,196
- References
- 139
- Citations by year
- 2026: 310 · 2025: 476 · 2024: 555 · 2023: 671 · 2022: 714 · 2021: 783 · 2020: 760 · 2019: 832 · 2018: 763 · 2017: 836 · 2016: 720 · 2015: 681 · 2014: 601 · 2013: 496 · 2012: 437
- FWCI
- 27.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Massachusetts Institute of Technology
- National Institutes of Health (DK 55001)
- Ludwig Center for Molecular Oncology
- Ludwig Center at Harvard
- National Institute on Alcohol Abuse and Alcoholism (AA 13913, R01AA013913)
- National Cancer Institute (U54 CA12515, R01CA125550, R01CA078461)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK61688, K08DK062978, DK-55001, R01DK061688, DK62978, R01DK055001)
- 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, mesenchymal cells, fibrosis, tumor invasion, metastasis, chronic inflammation, cancer, embryonic development, organogenesis, embryo implantation, signaling pathways, cellular plasticity, therapeutic interventions
- MeSH terms
- Animals, Cell Differentiation, Epithelial Cells, Fibrosis, Humans, Neoplasms, Regeneration, Mesenchymal Stem Cells
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