ReviewCells2020
Hybrid Epithelial/Mesenchymal State in Cancer Metastasis: Clinical Significance and Regulatory Mechanisms.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
78 citing papers in PubMed.
- Rosmarinic acid inhibits norepinephrine-induced metastatic capacity of triple negative breast cancer cells by Src kinase inactivation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Comparative Transcriptomic Analysis of Oral Squamous Cell Carcinoma with Progressive Cisplatin Resistance.International journal of molecular sciences · 2026Article
- Beyond Acute Infection: A Conceptual Framework Linking Zoonotic Bacterial Pathogens to Pulmonary Fibrosis and Lung Carcinogenesis.Biomedicines · 2026Review
- A guide to the types, structures, and multifaceted functions of matrix metalloproteinases in cancer.The FEBS journal · 2026Review
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- Histologic Heterogeneity of Metastases in Clear Cell Renal Cell Carcinoma with Sarcomatoid Differentiation.Journal of clinical medicine · 2026Article
- ANO1 stabilizes partial EMT to drive colorectal cancer metastasis through PI3K/AKT/mTOR and ERK signaling pathways.Scientific reports · 2026Article
- Hyperglycaemia-Induced Metabolic Stress Promotes EMT-Driven Therapeutic Resistance in Cancer: Evidence of a Deleterious Feed-Forward Cycle.Pharmaceuticals (Basel, Switzerland) · 2026Review
- A 3D model to evaluate cell chemotaxis within a heterogenic tumor microenvironment.Lab on a chip · 2026Article
- Review
- Electrospun PLA/PCL Composite Scaffolds as Platforms for Investigating Colorectal Cancer Cell Plasticity.ACS omega · 2026Article
- Circulating Tumor Cells: Emerging Frontiers in Cancer Technology.Expert reviews in molecular medicine · 2026Review
- Article
- A Novel Partial EMT-Associated Transcriptomic Signature for Prognostic Stratification in Ovarian Cancer.Oncology research · 2026Article
- Investigation of the possible effects of LncRNA CYTOR on the molecular mechanisms of metastasis and Hippo signaling pathways in Triple-negative and Cisplatin-resistant breast cancer cell lines.Medical oncology (Northwood, London, England) · 2025Article
- Circulating tumor cells as predictive biomarkers in the risk stratification of DCIS: Evidence of early dissemination.Science advances · 2025Article
- Differences in Expression of Epithelial-Mesenchymal Transition (EMT) Induction Genes TGF-Β Pathway Transition in Colorectal Cancer Patients Non-Metastatic and Metastatic.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Connexin43 functions as a non-canonical phenotypic stability factor in promoting hybrid Epithelial/Mesenchymal phenotype in glioblastoma cells.Translational oncology · 2025Article
- Upregulation ofInternational journal of molecular sciences · 2025Article
- Review
18 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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) has been well recognized for its essential role in cancer progression as well as normal tissue development. In cancer cells, activation of EMT permits the cells to acquire migratory and invasive abilities and stem-like properties. However, simple categorization of cancer cells into epithelial and mesenchymal phenotypes misleads the understanding of the complicated metastatic process, and contradictory results from different studies also indicate the limitation of application of EMT theory in cancer metastasis. Nowadays, growing evidence suggests the existence of an intermediate status between epithelial and mesenchymal phenotypes, i.e., the "hybrid epithelial-mesenchymal (hybrid E/M)" state, provides a possible explanation for those conflicting results. Appearance of hybrid E/M phenotype offers a more plastic status for cancer cells to adapt the stressful environment for proceeding metastasis. In this article, we review the biological importance of the dynamic changes between the epithelial and the mesenchymal states. The regulatory mechanisms encompassing the translational, post-translational, and epigenetic control for this complex and plastic status are also discussed.
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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.