ReviewJournal of clinical medicine2016
Role of EMT in Metastasis and Therapy Resistance.
Review in Journal of clinical medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 283 papers, 1 of them a synthesis that pooled it.
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
283 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular Biomarkers of Response to PD-1/ PD-L1 Immune Checkpoint Blockade in Advanced Bladder Cancer.Bladder cancer (Amsterdam, Netherlands) · 2019Pooled it
- Three-Course Neoadjuvant Chemotherapy Associated with Unfavorable Survival of Non-responders to the First Two Courses for Locally Advanced Esophageal Cancer.Annals of surgical oncology · 2023Trial
- Polarity protein Par3 deficiency promotes metastasis of bladder cancer via interaction of Ppp1r12c.Biology direct · 2026Article
- Adverse Outcome Pathway 298: Increase in Reactive Oxygen Species Leading to Human Treatment-Resistant Gastric Cancer.Cancers · 2026Article
- Article
- A Multiomics and Bioinformatics Analysis of the Role and Mechanism ofInternational journal of genomics · 2026Article
- Single-cell RNA sequencing reveals a quiescence-senescence continuum and distinct senotypes following chemotherapy.Nature communications · 2025Article
- Acyl-CoA dehydrogenase long chain acts as a tumor-suppressive factor in lung adenocarcinoma progression.Cell adhesion & migration · 2025Article
- Progerin regulates actin cytoskeletal remodeling and inhibits EMT and metastasis in triple‑negative breast cancer cells.International journal of oncology · 2025Article
- The role of SOX transcription factors in prostate cancer: Focusing on SOX2.Genes & diseases · 2025Review
- Cancer cell plasticity and therapeutic resistance: mechanisms, crosstalk, and translational perspectives.Hereditas · 2025Review
- Innovative Approaches to EMT-Related Biomarker Identification in Breast Cancer: Multi-Omics and Machine Learning Methods.Biotech (Basel (Switzerland)) · 2025Review
- 3D collagen high-throughput screen identifies drugs that induce epithelial polarity and enhance chemotherapy response in colorectal cancer.Communications biology · 2025Article
- Prediction of the effect of Bupleurum chinensis DC. (Chaihu) on survival and its potential targets in hepatocellular carcinoma based on a prognostic model.BMC complementary medicine and therapies · 2025Article
- Multiple roles of S100P in pan carcinoma: Biological functions and mechanisms (Review).Oncology reports · 2025Review
- Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Review
- Exploring the role of EMT in ovarian cancer progression using a multiscale mathematical model.NPJ systems biology and applications · 2025Article
- Effects ofMarine drugs · 2025Article
- CIP2A promotes bronchiolitis obliterans by activating the NF‑κB pathway.Molecular medicine reports · 2025Article
223 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
Abstract
Epithelial-mesenchymal transition (EMT) is a complex molecular program that regulates changes in cell morphology and function during embryogenesis and tissue development. EMT also contributes to tumor progression and metastasis. Cells undergoing EMT expand out of and degrade the surrounding microenvironment to subsequently migrate from the primary site. The mesenchymal phenotype observed in fibroblasts is specifically important based on the expression of smooth muscle actin (α-SMA), fibroblast growth factor (FGF), fibroblast-specific protein-1 (FSP1), and collagen to enhance EMT. Although EMT is not completely dependent on EMT regulators such as Snail, Twist, and Zeb-1/-2, analysis of upstream signaling (i.e., TGF-β, EGF, Wnt) is necessary to understand tumor EMT more comprehensively. Tumor epithelial-fibroblast interactions that regulate tumor progression have been identified during prostate cancer. The cellular crosstalk is significant because these events influence therapy response and patient outcome. This review addresses how canonical EMT signals originating from prostate cancer fibroblasts contribute to tumor metastasis and recurrence after therapy.
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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.