ArticleOncogene2021
Isolating and targeting the real-time plasticity and malignant properties of epithelial-mesenchymal transition in cancer.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 23 citations in OpenAlex.
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- Dynamic Interplay of Epithelial-Mesenchymal and Mesenchymal-Epithelial Transitions in Cochlear Development and Disease: Molecular Mechanisms and Therapeutic Implications.Biomedicines · 2025Review
- Construction of Metastasis Prediction Models and Screening of Anti-Metastatic Drugs Based on Pan-Cancer Single-Cell EMT Features.International journal of molecular sciences · 2025Article
- CHD1L in cancer and beyond: structure, oncogenic functions, and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025Review
- Twist-Induced Epithelial-to-Mesenchymal Transition Confers Specific Metabolic and Mitochondrial Alterations.Cells · 2025Article
- Bridging the gap: the role of 3D cell cultures in mimicking tumor microenvironment for enhanced drug testing accuracy.Frontiers in bioengineering and biotechnology · 2025Review
- Periostin Induces Epithelial-Mesenchymal Transition via p38-MAPK Pathway in Human Renal Tubular Cells by High Glucose.Immunity, inflammation and disease · 2024Article
- Identification and Characterization of Metastasis-Initiating Cells in ESCC in a Multi-Timepoint Pulmonary Metastasis Mouse Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Targeting the key players of phenotypic plasticity in cancer cells by phytochemicals.Cancer metastasis reviews · 2024Review
- The first embryo, the origin of cancer and animal phylogeny. II. The neoplastic process as an evolutionary engine.Journal of biosciences · 2024Article
- The validation of new CHD1L inhibitors as a therapeutic strategy for cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- Review
- Neural induction drives body axis formation during embryogenesis, but a neural induction-like process drives tumorigenesis in postnatal animals.Frontiers in cell and developmental biology · 2023Review
- Regulation of TGF-Cancers · 2022Article
- High-Content Drug Discovery Targeting Molecular Bladder Cancer Subtypes.International journal of molecular sciences · 2022Article
- Traject3d allows label-free identification of distinct co-occurring phenotypes within 3D culture by live imaging.Nature communications · 2022Article
- Article
- Design, Synthesis, and Biological Evaluation of the First Inhibitors of Oncogenic CHD1L.Journal of medicinal chemistry · 2022Article
- Desensitization of human breast progenitors by a transient exposure to pregnancy levels of estrogen.Scientific reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) is a driving force in promoting malignant cancer, including initiation, growth, and metastasis. EMT is a dynamic process that can undergo a mesenchymal-epithelial transition (MET) and partial transitions between both phenotypes, termed epithelial-mesenchymal plasticity (EMP). In cancer, the acquisition of EMP results in a spectrum of phenotypes, promoting tumor cell heterogeneity and resistance to standard of care therapy. Here we describe a real-time fluorescent dual-reporter for vimentin and E-cadherin, biomarkers of the mesenchymal and epithelial cell phenotypes, respectively. Stable dual-reporter cell lines generated from colorectal (SW620), lung (A549), and breast (MDA-MB-231) cancer demonstrate a spectrum of EMT cell phenotypes. We used the dual-reporter to isolate the quasi epithelial, epithelial/mesenchymal, and mesenchymal phenotypes. Although EMT is a dynamic process, these isolated quasi-EMT-phenotypes remain stable to spontaneous EMP in the absence of stimuli and during prolonged cell culture. However, the quasi-EMT phenotypes can readily be induced to undergo EMT or MET with growth factors or small molecules. Moreover, isolated EMT phenotypes display different tumorigenic properties and are morphologically and metabolically distinct. 3D high-content screening of ~23,000 compounds using dual-reporter mesenchymal SW620 tumor organoids identified small molecule probes that modulate EMT, and a subset of probes that effectively induced MET. The tools, probes, and models described herein provide a coherent mechanistic understanding of mesenchymal cell plasticity. Future applications utilizing this technology and probes are expected to advance our understanding of EMT and studies aimed at therapeutic strategies targeting EMT.
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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.