ArticleFrontiers in cell and developmental biology2014
Epithelial to mesenchymal transition in tumor cells as consequence of phenotypic instability.
Article in Frontiers in cell and developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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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
9 citing papers in PubMed, 14 citations in OpenAlex.
- Histological and Immunohistochemical Studies to Determine the Mechanism of Cleft Palate Induction after Palatal Fusion in Mice Exposed to TCDD.International journal of molecular sciences · 2022Article
- The Inflammatory Profile of the Tumor Microenvironment, Orchestrated by Cyclooxygenase-2, Promotes Epithelial-Mesenchymal Transition.Frontiers in oncology · 2021Review
- Article
- Systemic Metabolism, Its Regulators, and Cancer: Past Mistakes and Future Potential.Frontiers in endocrinology · 2019Review
- Withaferin A inhibits Epithelial to Mesenchymal Transition in Non-Small Cell Lung Cancer Cells.Scientific reports · 2018Article
- Article
- Article
- OVOL guides the epithelial-hybrid-mesenchymal transition.Oncotarget · 2015Article
- Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis.Frontiers in oncology · 2015Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the last years many articles have reported epithelial-to-mesenchymal transitions (EMT) induced by a myriad of gene products either when added to the cell medium or when transfected. Molecularly the EMT is characterized by the up-regulation of transcriptional factors (EMT-TFs) repressing the epithelial gene E-cadherin, a protein essential for the maintenance of the epithelial phenotype. These EMT-TFs are subjected to a complex regulation involving binary self-stimulatory loops, allowing the possibility of the amplification of input signals. The capability of EMT-TFs to promote an EMT is controlled by E-cadherin that limits the transcription of mesenchymal genes. We discuss here the differences between normal and tumor epithelial cells; in the latter a partial inactivation of E-cadherin function enables extracellular signals to be amplified and induce an EMT. This tumor cell phenotypic instability is exacerbated in cell culture conditions. Therefore, it is likely that many of the gene products reported to control this transition act only in very specific cell tumor cell lines; thus, in cells with an unstable phenotype due to pre-existing alterations in E-cadherin safeguard mechanism.
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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.