ArticlePloS one2012
A cell-based small molecule screening method for identifying inhibitors of epithelial-mesenchymal transition in carcinoma.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 79 citations in OpenAlex.
- Review
- The impact of epithelial-mesenchymal transition (EMT) induced by metabolic processes and intracellular signaling pathways on chemo-resistance, metastasis, and recurrence in solid tumors.Cell communication and signaling : CCS · 2024Review
- Can Natural Products Targeting EMT Serve as the Future Anticancer Therapeutics?Molecules (Basel, Switzerland) · 2022Review
- Review
- EMT signaling: potential contribution of CRISPR/Cas gene editing.Cellular and molecular life sciences : CMLS · 2020Review
- Targeting codon 158 p53-mutant cancers via the induction of p53 acetylation.Nature communications · 2020Article
- Secondary Metabolites from the Culture of the Marine-derived FungusMarine drugs · 2020Article
- Recent Advances in Cancer Plasticity: Cellular Mechanisms, Surveillance Strategies, and Therapeutic Optimization.Frontiers in oncology · 2020Review
- Sanguinarine inhibits epithelial-mesenchymal transition via targeting HIF-1α/TGF-β feed-forward loop in hepatocellular carcinoma.Cell death & disease · 2019Article
- c-Met activation leads to the establishment of a TGFβ-receptor regulatory network in bladder cancer progression.Nature communications · 2019Article
- Actin cytoskeleton self-organization in single epithelial cells and fibroblasts under isotropic confinement.Journal of cell science · 2019Article
- The tumour suppressor OPCML promotes AXL inactivation by the phosphatase PTPRG in ovarian cancer.EMBO reports · 2018Article
- Cellular Phenotype Plasticity in Cancer Dormancy and Metastasis.Frontiers in oncology · 2018Review
- Integration of pan-cancer transcriptomics with RPPA proteomics reveals mechanisms of epithelial-mesenchymal transition.PLoS computational biology · 2018Article
- The EMT spectrum and therapeutic opportunities.Molecular oncology · 2017Review
- New insights into the role of EMT in tumor immune escape.Molecular oncology · 2017Review
- Pharmacological and immunological targeting of tumor mesenchymalization.Pharmacology & therapeutics · 2017Review
- Article
- Therapeutic Targeting of Epithelial Plasticity Programs: Focus on the Epithelial-Mesenchymal Transition.Cells, tissues, organs · 2017Review
- Targeting Estrogen Receptor Signaling with Fulvestrant Enhances Immune and Chemotherapy-Mediated Cytotoxicity of Human Lung Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial Mesenchymal Transition (EMT) is a crucial mechanism for carcinoma progression, as it provides routes for in situ carcinoma cells to dissociate and become motile, leading to localized invasion and metastatic spread. Targeting EMT therefore represents an important therapeutic strategy for cancer treatment. The discovery of oncogene addiction in sustaining tumor growth has led to the rapid development of targeted therapeutics. Whilst initially optimized as anti-proliferative agents, it is likely that some of these compounds may inhibit EMT initiation or sustenance, since EMT is also modulated by similar signaling pathways that these compounds were designed to target. We have developed a novel screening assay that can lead to the identification of compounds that can inhibit EMT initiated by growth factor signaling. This assay is designed as a high-content screening assay where both cell growth and cell migration can be analyzed simultaneously via time-course imaging in multi-well plates. Using this assay, we have validated several compounds as viable EMT inhibitors. In particular, we have identified compounds targeting ALK5, MEK, and SRC as potent inhibitors that can interfere with EGF, HGF, and IGF-1 induced EMT signaling. Overall, this EMT screening method provides a foundation for improving the therapeutic value of recently developed compounds in advanced stage carcinoma.
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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.