ReviewJAK-STAT2014
STAT3 and epithelial-mesenchymal transitions in carcinomas.
Review in JAK-STAT, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 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
137 citing papers in PubMed, 201 citations in OpenAlex.
- TNF overproduction impairs epithelial staphylococcal response in hyper IgE syndrome.The Journal of clinical investigation · 2018Trial
- Multi-Modal Kinome Profiling Discovers Mesenchymal-Like Polarity Networks that Underly Directed Hepatocellular Carcinoma Cell Migration.bioRxiv : the preprint server for biology · 2026Article
- Decoy oligonucleotide technology in cancer therapy: molecular mechanisms, challenges, and translational potential.Medical oncology (Northwood, London, England) · 2026Review
- Systematic analyses to explore kinase gene set-based signature in glioma, in which WEE1 contributes to tumor progression.Discover oncology · 2026Article
- Activation of STAT3 in the COPD airway epithelium.ERJ open research · 2026Article
- Modulators of epithelial-mesenchymal transitions in prostate cancer: potential for novel therapeutics development.Frontiers in pharmacology · 2026Article
- ARID1A deficiency activates OSM-STAT3 axis in endometrial cancer, creating vulnerability to JAK/STAT3 inhibition.International journal of biological sciences · 2026Article
- Isoalantolactone Attenuates LPS-Induced Acute Lung Injury, an Effect Associated with Suppressed MAPK/STAT3 Activation and Epithelial-Mesenchymal Transition.International journal of medical sciences · 2026Article
- POC1A induces epithelial-mesenchymal transition to promote growth and metastasis through the STAT3 signaling pathway in triple-negative breast cancer.Molecular medicine (Cambridge, Mass.) · 2025Article
- The kinase ERK plays a conserved dominant role in the heterogeneity of epithelial-mesenchymal transition in pancreatic cancer cells.Science signaling · 2025Article
- Review
- Effects of SB939 are mediated by STAT3 to inhibit breast cancer cell metastasis-related genes.Oncology letters · 2025Article
- STAT3 inhibition in combination with CD47 blockade inhibits osteosarcoma lung metastasis.Frontiers in immunology · 2025Article
- Small Molecule with Big Impact: Metarrestin Targets the Perinucleolar Compartment in Cancer Metastasis.Cells · 2024Review
- Effect of Soy Isoflavone on Prostate Cancer Cell Apoptosis Through Inhibition of STAT3, ERK, and AKT.Current issues in molecular biology · 2024Article
- The plasma EBV DNA load with IL-6 and VEGF levels as predictive and prognostic biomarker in nasopharyngeal carcinoma.Virology journal · 2024Article
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- TCAF2 drives glioma cellular migratory/invasion properties through STAT3 signaling.Molecular and cellular biochemistry · 2024Article
- Crosstalk between CAFs and tumour cells in head and neck cancer.Cell death discovery · 2024Review
77 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 2 institutions in 1 country.
Funding
Abstract
Cellular programs coupled to cycles of epithelial-mesenchymal transitions (EMTs) play critical roles during embryogenesis, as well as during tissue development, remodeling, and repair. Research over the last decade has established the importance of an ever-expanding list of master EMT transcription factors, whose activity is regulated by STAT3 and function to stimulate the rapid transition of cells between epithelial and mesenchymal phenotypes. Importantly, inappropriate reactivation of embryonic EMT programs in carcinoma cells underlies their metastasis to distant organ sites, as well as their acquisition of stem cell-like and chemoresistant phenotypes operant in eliciting disease recurrence. Thus, targeted inactivation of master EMT transcription factors may offer new inroads to alleviate metastatic disease. Here we review the molecular, cellular, and microenvironmental factors that contribute to the pathophysiological activities of STAT3 during its regulation of EMT programs in human carcinomas.
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.