Epithelial Mesenchymal Transition in Tumor Metastasis
Open accessAbstract
Metastasis is the major cause of cancer-related deaths; therefore, the prevention and treatment of metastasis are fundamental to improving clinical outcomes. Epithelial mesenchymal transition (EMT), an evolutionarily conserved developmental program, has been implicated in carcinogenesis and confers metastatic properties upon cancer cells by enhancing mobility, invasion, and resistance to apoptotic stimuli. Furthermore, EMT-derived tumor cells acquire stem cell properties and exhibit marked therapeutic resistance. Given these attributes, the complex biological process of EMT has been heralded as a key hallmark of carcinogenesis, and targeting EMT pathways constitutes an attractive strategy for cancer treatment. However, demonstrating the necessity of EMT for metastasis in vivo has been technically challenging, and recent efforts to demonstrate a functional contribution of EMT to metastasis have yielded unexpected results. Therefore, determining the functional role of EMT in metastasis remains an area of active investigation. Studies using improved lineage tracing systems, dynamic in vivo imaging, and clinically relevant in vivo models have the potential to uncover the direct link between EMT and metastasis. This review focuses primarily on recent advances in and emerging concepts of the biology of EMT in metastasis in vivo and discusses future directions in the context of novel diagnostic and therapeutic opportunities.
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EMT 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 [33]
The Introduction (page unavailable) lists Wnt/β-catenin among pathways that regulate EMT, and the Primary Tumors section describes mesenchymal properties that enable migration and invasion. But the paper does not establish that Wnt/β-catenin *frequently* regulates EMT. The Monitoring Along the Metastatic Cascade In Vivo section also cautions that EMT’s necessity for metastasis is unproven, making “a hallmark of metastasis” too categorical. (LLM, conf=0.88)
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Cites
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- Authors
- Mittal, V.
- Affiliations
- Weill Cornell Medicine (US)
- Corresponding author
- Mittal, Vivek
- ORCID
- Mittal, Vivek
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2018-01-24
- Volume
- 13
- Issue
- 1
- Pages
- 395-412
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- OpenAlex
- W2786843484
- Cited by
- 1,528
- References
- 6
- Citations by year
- 2026: 101 · 2025: 191 · 2024: 251 · 2023: 275 · 2022: 273 · 2021: 207 · 2020: 140 · 2019: 64 · 2018: 23 · 2017: 2
- FWCI
- 11.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- 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 › Mechanisms of cancer metastasis
- Keywords
- epithelial-mesenchymal transition, metastasis, cancer stemness, treatment resistance, tumor invasion, tumor cell motility, carcinogenesis, lineage tracing
- MeSH terms
- Humans, Neoplasm Invasiveness, Neoplasms, Epithelial-Mesenchymal Transition
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