ReviewInternational journal of molecular sciences2018
Epithelial-Mesenchymal Transition and Metastasis under the Control of Transforming Growth Factor β.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
107 citing papers in PubMed, 155 citations in OpenAlex.
- AdipoRon Modulation of the Invasive Potential of Prostate Cancer Cells Is Dependent on Their EMT-Related Phenotype.Biomedicines · 2026Article
- COMP-PMEPA1 axis promotes epithelial-to-mesenchymal transition in breast cancer cells.Molecular oncology · 2026Article
- Rewiring miR-22/SNAI1 via CRISPR-based edge editing destabilizes the epithelial phenotype.NPJ systems biology and applications · 2026Article
- Macrophage plasticity in the osteosarcoma tumor microenvironment: opportunities and challenges for immunotherapy.Journal of cancer research and clinical oncology · 2026Review
- Astragalus Polysaccharide Attenuates Breast Cancer Progression by Regulating METTL3-Mediated MAL2 mJournal of microbiology and biotechnology · 2026Article
- Exploring Molecular Mechanism of Thymoquinone via cMet and PDGFR for Accelerated Hemostasis: An Approach Through In Silico, In Vitro, and In Vivo Studies.Chemistry & biodiversity · 2026Article
- Konjac petroleum ether extract inhibits triple-negative breast cancer cell migration and invasion by attenuatingFrontiers in pharmacology · 2026Article
- The Redox-Adhesion-Exosome (RAX) Hub in Cancer: Lipid Peroxidation-Driven EMT Plasticity and Ferroptosis Defense with HNE/MDA Signaling and Lipidomic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Liver metastasis of colorectal cancer: Mechanism and clinical therapy (Review).Oncology reports · 2025Review
- The Potential Role ofMicroorganisms · 2025Review
- Low BOK Expression Promotes Epithelial-Mesenchymal Transition and Migration via the Wnt Signaling Pathway in Breast Cancer Cells.International journal of molecular sciences · 2025Article
- Immune factors and their role in tumor aggressiveness in glioblastoma: Atypical cadherin FAT1 as a promising target for combating immune evasion.Cellular & molecular biology letters · 2025Review
- Review
- Multi-omics analysis of copper metabolism-related molecular subtypes and risk stratification for osteosarcoma.Discover oncology · 2025Article
- Promotion of human choroidal melanoma cell metastases by FOXP3International journal of ophthalmology · 2025Article
- Osteosarcoma immune microenvironment: cellular struggle and novel therapeutic insights.Frontiers in immunology · 2025Review
- Review
- The Inhibitory Effect and Mechanism of the Histidine-Rich Peptide rAj-HRP fromMolecules (Basel, Switzerland) · 2024Article
- Exosomes on the development and progression of renal fibrosis.Cell proliferation · 2024Review
- Advances on immunotherapy for osteosarcoma.Molecular cancer · 2024Review
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Metastasis of tumor cells from primary sites of malignancy to neighboring stromal tissue or distant localities entails in several instances, but not in every case, the epithelial-mesenchymal transition (EMT). EMT weakens the strong adhesion forces between differentiated epithelial cells so that carcinoma cells can achieve solitary or collective motility, which makes the EMT an intuitive mechanism for the initiation of tumor metastasis. EMT initiates after primary oncogenic events lead to secondary secretion of cytokines. The interaction between tumor-secreted cytokines and oncogenic stimuli facilitates EMT progression. A classic case of this mechanism is the cooperation between oncogenic Ras and the transforming growth factor β (TGFβ). The power of TGFβ to mediate EMT during metastasis depends on versatile signaling crosstalk and on the regulation of successive waves of expression of many other cytokines and the progressive remodeling of the extracellular matrix that facilitates motility through basement membranes. Since metastasis involves many organs in the body, whereas EMT affects carcinoma cell differentiation locally, it has frequently been debated whether EMT truly contributes to metastasis. Despite controversies, studies of circulating tumor cells, studies of acquired chemoresistance by metastatic cells, and several (but not all) metastatic animal models, support a link between EMT and metastasis, with TGFβ, often being a common denominator in this link. This article aims at discussing mechanistic cases where TGFβ signaling and EMT facilitate tumor cell dissemination.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.