ReviewTranslational oncology2020
Hypoxia, partial EMT and collective migration: Emerging culprits in metastasis.
Review in Translational oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 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
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Who cites it
114 citing papers in PubMed, 211 citations in OpenAlex.
- Adjuvant therapies by anthocyanins potentially mitigating drug resistance and metastatic disease risks in stratified breast cancers: the 3PM-conceptual innovation targeted to NF-kappaB/EMT plasticity.The EPMA journal · 2026Article
- Association of glycolysis-related protein expression with prognosis in Canine Pulmonary Adenocarcinoma.The Journal of veterinary medical science · 2026Article
- Hypoxia-inducible factors: Regulatory functions and status as a therapeutic target in gastric cancer (Review).Oncology letters · 2026Review
- Article
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- Time-dependent memory of hypoxia exposure influences tumor invasion dynamics.bioRxiv : the preprint server for biology · 2026Article
- ANKRD49 promotes the epithelial-mesenchymal transition of non-small cell lung cancer via the PKNOX1/TGF-β1/SMAD axis.Cancer cell international · 2026Article
- Article
- Recognition of immunogenomic signature and prognostic value of the subtype of epithelial-mesenchymal transition in breast cancer.Biochemistry and biophysics reports · 2026Article
- Hypoxia-inducible factor 1α exerts dual roles in bladder cancer progression through TIMP3-mediated regulation of angiogenesis and invasion.Scientific reports · 2026Article
- Partial-EMT in oral squamous cell carcinoma: molecular circuitry and clinical translation.International journal of oral science · 2026Review
- A Novel Partial EMT-Associated Transcriptomic Signature for Prognostic Stratification in Ovarian Cancer.Oncology research · 2026Article
- Polycyclic aromatic hydrocarbon derivative 3-hydroxybenz[a]anthracene promotes the progression of T47D breast cancer cells by modulating relevant protein expression.Frontiers in cell and developmental biology · 2026Article
- Single-cell multiomic modelling of early metastatic events promoted by the extracellular matrix.British journal of cancer · 2025Article
- Hirudin suppresses hematogenous metastasis by targeting desmosome junction transition in circulating tumor cell clusters via HIF-1α-DSG2 signaling.Experimental & molecular medicine · 2025Article
- HOXA10-TWIST2 antagonism drives partial epithelial-to-mesenchymal transition for embryo implantation.Cell death discovery · 2025Article
- Shared and Context-Specific Mechanisms of EMT and Cellular Plasticity in Cancer and Fibrotic Diseases.International journal of molecular sciences · 2025Review
- Oncostatin M orchestrates collective epithelial migration via HIF1A activation.bioRxiv : the preprint server for biology · 2025Article
- History of hypoxia exposure aids future cell invasion according to cell type and collagen density.Molecular biology of the cell · 2025Article
- High hypoxia inducible factor-1α expression is associated with reduced survival in patients with breast cancer: A meta-analysis.World journal of clinical oncology · 2025Article
54 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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is a cellular biological process involved in migration of primary cancer cells to secondary sites facilitating metastasis. Besides, EMT also confers properties such as stemness, drug resistance and immune evasion which can aid a successful colonization at the distant site. EMT is not a binary process; recent evidence suggests that cells in partial EMT or hybrid E/M phenotype(s) can have enhanced stemness and drug resistance as compared to those undergoing a complete EMT. Moreover, partial EMT enables collective migration of cells as clusters of circulating tumor cells or emboli, further endorsing that cells in hybrid E/M phenotypes may be the 'fittest' for metastasis. Here, we review mechanisms and implications of hybrid E/M phenotypes, including their reported association with hypoxia. Hypoxia-driven activation of HIF-1α can drive EMT. In addition, cyclic hypoxia, as compared to acute or chronic hypoxia, shows the highest levels of active HIF-1α and can augment cancer aggressiveness to a greater extent, including enriching for a partial EMT phenotype. We also discuss how metastasis is influenced by hypoxia, partial EMT and collective cell migration, and call for a better understanding of interconnections among these mechanisms. We discuss the known regulators of hypoxia, hybrid EMT and collective cell migration and highlight the gaps which needs to be filled for connecting these three axes which will increase our understanding of dynamics of metastasis and help control it more effectively.
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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.