ArticlePloS one2012
FGFR1-induced epithelial to mesenchymal transition through MAPK/PLCγ/COX-2-mediated mechanisms.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 92 citations in OpenAlex.
- Ectodermal loss of ARHGAP29 alters epithelial morphology and disrupts murine palatogenesis.Development (Cambridge, England) · 2026Article
- Review
- Repurposing the Tyrosine Kinase Inhibitors Targeting FGFR and VEGFR Pathways for Cancer Therapy: A Comprehensive Review.Cancers · 2025Review
- Intercellular signaling reinforces single-cell level phenotypic transitions and facilitates robust re-equilibrium of heterogeneous cancer cell populations.Cell communication and signaling : CCS · 2025Article
- The FGFR inhibitor pemigatinib overcomes cancer drug resistance to KRAS G12C inhibitors in mesenchymal lung cancer.PloS one · 2025Article
- Characterization of cancer-related fibroblasts in bladder cancer and construction of CAFs-based bladder cancer classification: insights from single-cell and multi-omics analysis.Frontiers in immunology · 2025Article
- Expression of fibroblast growth factor receptor 1 correlates inversely with the efficacy of single-agent fibroblast growth factor receptor-specific inhibitors in pancreatic cancer.British journal of pharmacology · 2024Article
- Landscape of targeted therapies for advanced urothelial carcinoma.Exploration of targeted anti-tumor therapy · 2024Review
- Shake It Up Baby Now: The Changing Focus on TWIST1 and Epithelial to Mesenchymal Transition in Cancer and Other Diseases.International journal of molecular sciences · 2023Review
- Bladder cancer.Nature reviews. Disease primers · 2023Review
- Spatial distribution and functional relevance of FGFR1 and FGFR2 expression for glioblastoma tumor invasion.Cancer letters · 2023Article
- Article
- Digital lamellar inflammatory signaling in an experimental model of equine preferential weight bearing.Journal of veterinary internal medicine · 2023Article
- Nonsteroidal anti-inflammatory drugs and implications for the cyclooxygenase pathway in embryonic development.American journal of physiology. Cell physiology · 2023Review
- Inflammation in Urological Malignancies: The Silent Killer.International journal of molecular sciences · 2023Review
- Overarching roles of diacylglycerol signaling in cancer development and antitumor immunity.Science signaling · 2022Review
- Review
- Epithelial-mesenchymal transition and its transcription factors.Bioscience reports · 2022Review
- The Warburg effect as a therapeutic target for bladder cancers and intratumoral heterogeneity in associated molecular targets.Cancer science · 2021Article
- Synthetic dysmobility screen unveils an integrated STK40-YAP-MAPK system driving cell migration.Science advances · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Tumour invasion and metastasis is the most common cause of death from cancer. For epithelial cells to invade surrounding tissues and metastasise, an epithelial-mesenchymal transition (EMT) is required. We have demonstrated that FGFR1 expression is increased in bladder cancer and that activation of FGFR1 induces an EMT in urothelial carcinoma (UC) cell lines. Here, we created an in vitro FGFR1-inducible model of EMT, and used this model to identify regulators of urothelial EMT. FGFR1 activation promoted EMT over a period of 72 hours. Initially a rapid increase in actin stress fibres occurred, followed by an increase in cell size, altered morphology and increased migration and invasion. By using site-directed mutagenesis and small molecule inhibitors we demonstrated that combined activation of the mitogen activated protein kinase (MAPK) and phospholipase C gamma (PLCγ) pathways regulated this EMT. Actin stress fibre formation was regulated by PLCγ activation, and was also important for the increase in cell size, migration and altered morphology. MAPK activation regulated migration and E-cadherin expression, indicating that combined activation of PLCγ and MAPK is required for a full EMT. We used expression microarrays to assess changes in gene expression downstream of these signalling cascades. COX-2 was transcriptionally upregulated by FGFR1 and caused increased intracellular prostaglandin E(2) levels, which promoted migration. In conclusion, we have demonstrated that FGFR1 activation in UC cells lines promotes EMT via coordinated activation of multiple signalling pathways and by promoting activation of prostaglandin synthesis.
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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.