ReviewCancer research2009
Epithelial-mesenchymal transition and cell cooperativity in metastasis.
Review in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 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
226 citing papers in PubMed, 409 citations in OpenAlex.
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- Mechanisms Underlying the Initiation and Termination of Collective Cell Migration: Perspectives for Understanding Development and Cancer Metastasis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Spatial gene expression analysis reveals drivers of extremely early lymph node metastasis in breast cancer.NPJ breast cancer · 2026Article
- Detection of Circulating Tumor Cells with an Epithelial-to-Mesenchymal Transition Phenotype.Methods in molecular biology (Clifton, N.J.) · 2026Article
- F-actin dynamics regulates collective cell migration by modulating cell shape and stress correlation.Biophysical journal · 2025Article
- Plasma-Derived Exosomal i-tRF-LeuCAA as Biomarker for Glioma Diagnosis and Promoter of Epithelial-Mesenchymal Transition via TPM4 Regulation.CNS neuroscience & therapeutics · 2025Article
- Comparative Analysis of Transcription Factors TWIST2, GATA3, and HES5 in Glioblastoma Multiforme : Evaluating Biomarker Potential and Therapeutic Targets Using in Silico Methods.Journal of Korean Neurosurgical Society · 2025Article
- Advances in microfluidic platforms for tumor cell phenotyping: from bench to bedside.Lab on a chip · 2025Review
- SATB1 in cancer progression and metastasis: mechanisms and therapeutic potential.Frontiers in oncology · 2025Review
- IRTKS contributes to the malignant progression of cervical cancer cells.Medical oncology (Northwood, London, England) · 2024Article
- Long Non-Coding RNAs in Drug Resistance of Gastric Cancer: Complex Mechanisms and Potential Clinical Applications.Biomolecules · 2024Review
- The dynamic tumor-stromal crosstalk: implications of 'stromal-hot' tumors in the process of epithelial-mesenchymal transition in breast cancer.Molecular biology reports · 2023Review
- Regulation of Cancer Stem Cells and Epithelial-Mesenchymal Transition by CTNNAL1 in Lung Cancer and Glioblastoma.Biomedicines · 2023Article
- Significance of circulating tumor cells in lung cancer: a narrative review.Translational lung cancer research · 2023Review
- Persistence Infection of TGEV PromotesInternational journal of molecular sciences · 2022Article
- MicroRNA-Gene Interactions Impacted by Toxic Metal(oid)s during EMT and Carcinogenesis.Cancers · 2022Review
- Article
- Ginsenoside Rh3 Inhibits Lung Cancer Metastasis by Targeting Extracellular Signal-Regulated Kinase: A Network Pharmacology Study.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Stanniocalcin 2 (STC2): a universal tumour biomarker and a potential therapeutical target.Journal of experimental & clinical cancer research : CR · 2022Review
- Article
166 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
3 authors at 3 institutions in 2 countries.
Funding
Abstract
The role of epithelial-mesenchymal transition (EMT) in metastasis remains controversial. EMT has been postulated as an absolute requirement for tumor invasion and metastasis. Three different models including incomplete EMT, mesenchymal-epithelial transition (MET), and collective migration have been proposed for the role of EMT in cancer invasion and metastasis. However, skepticism remains about whether EMT truly occurs during cancer progression, and if it does, whether it plays an indispensible role in metastasis. Our recent findings suggest that EMT cells are responsible for degrading the surrounding matrix to enable invasion and intravasation of both EMT and non-EMT cells. Only non-EMT cells that have entered the blood stream are able to re-establish colonies in the secondary sites. Here, we discuss an alternative model for the role of EMT in cancer metastasis in which EMT and non-EMT cells cooperate to complete the entire process of spontaneous metastasis.
Indexed as
Identifiers
What OpenQuestion holds
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.