ReviewMolecular cancer2023
EMT/MET plasticity in cancer and Go-or-Grow decisions in quiescence: the two sides of the same coin?
Review in Molecular cancer, 2023. 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
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
114 citing papers in PubMed, 143 citations in OpenAlex.
- The H63D Polymorphism in the HFE Gene Promotes Aggressive Disease Phenotypes in Pancreatic Ductal Adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- HSPE1 promotes immune evasion in lung adenocarcinoma by mediating mitochondrial oxidative stress via histone lactylation-mediated SDHA transcriptional activation.Translational oncology · 2026Article
- Adaptive epithelial-mesenchymal bi-directional transition: A key invasive plasticity for tumor metastasis.iScience · 2026Review
- Article
- EDNRB-dependent endothelin signaling reduces proliferation and promotes proneural-to-mesenchymal transition in gliomas.Molecular oncology · 2026Article
- Matricellular Proteins in Bladder Cancer: Context-Dependent Roles in Tumor Promotion and Suppression.International journal of molecular sciences · 2026Review
- Copper homeostasis and cuproptosis rewire the tumor microenvironment: mechanisms, immune modulation, and therapeutic opportunities.Journal of hematology & oncology · 2026Review
- Spatial ecology of breast cancer reveals co-evolution of proliferative and dormant niches.Genome medicine · 2026Article
- Spatial transcriptomic profiling of ovarian clear cell carcinoma reveals heterogeneity in OXPHOS and EMT gradients.Nature communications · 2026Article
- Spatiotemporal organisation of residual disease in mouse and human BRCA1-deficient mammary tumours and breast cancer.Nature communications · 2026Article
- Unveiling LAIR1: a prognostic biomarker associated with gastric cancer progression and metastasis.Translational cancer research · 2026Article
- Cycle-consistent deep generative modeling unifies cellular states across unpaired spatial and single-cell modalities.bioRxiv : the preprint server for biology · 2026Article
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- Pancreatic cancer EMT‑targeted therapy: Molecular mechanisms and clinical translation (Review).International journal of oncology · 2026Review
- Cholesterol synthases suppress metastasis and stemness through PDIA4/ACLY or SYVN1/SCD1 axis in advanced colorectal cancer.Communications biology · 2026Article
- PMEPA1 modulates YAP1 nuclear translocation to disrupt EMT subtypes and promote metastasis in Biliary tract cancer.Cell death & disease · 2026Article
- Cellular Identity Crisis: RD3 Loss Fuels Plasticity and Immune Silence in Progressive Neuroblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Human Amniotic Mesenchymal Stromal Cells Promote Bone Regeneration via Regulating Ameloblastoma-Derived-Bone Marrow Mesenchymal Cells Crosstalk and Autophagy in Ameloblastoma Microenvironment.Tissue engineering and regenerative medicine · 2026Article
- Circular RNA MALAT1 as a potential target for antimetastatic therapy.Non-coding RNA research · 2026Review
- FNDC1 Competitively Binds Gβ2 to Suppress the β-Catenin-Destruction Complex and Promote Gastric Cancer Malignancy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial mesenchymal transition (EMT) and mesenchymal epithelial transition (MET) are genetic determinants of cellular plasticity. These programs operate in physiological (embryonic development, wound healing) and pathological (organ fibrosis, cancer) conditions. In cancer, EMT and MET interfere with various signalling pathways at different levels. This results in gross alterations in the gene expression programs, which affect most, if not all hallmarks of cancer, such as response to proliferative and death-inducing signals, tumorigenicity, and cell stemness. EMT in cancer cells involves large scale reorganisation of the cytoskeleton, loss of epithelial integrity, and gain of mesenchymal traits, such as mesenchymal type of cell migration. In this regard, EMT/MET plasticity is highly relevant to the Go-or-Grow concept, which postulates the dichotomous relationship between cell motility and proliferation. The Go-or-Grow decisions are critically important in the processes in which EMT/MET plasticity takes the central stage, mobilisation of stem cells during wound healing, cancer relapse, and metastasis. Here we outline the maintenance of quiescence in stem cell and metastatic niches, focusing on the implication of EMT/MET regulatory networks in Go-or-Grow switches. In particular, we discuss the analogy between cells residing in hybrid quasi-mesenchymal states and G
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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.