ArticlePloS one2019
Addiction of mesenchymal phenotypes on the FGF/FGFR axis in oral squamous cell carcinoma cells.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- The ARTEMIS trial identifies immune activation as a key predictor of neoadjuvant chemotherapy response in triple-negative breast cancer.Breast cancer research : BCR · 2026Trial
- The role of homeobox genes in signaling pathway positive feedback loops and cancer therapy.Frontiers in oncology · 2026Article
- The role of ESRP1 in solid tumor development through the regulation of CD44 splicing and EMT processes.Frontiers in oncology · 2025Review
- Roles of ZEB1 and ZEB2 in E-cadherin expression and cell aggressiveness in head and neck cancer.Genes to cells : devoted to molecular & cellular mechanisms · 2024Article
- Comprehensive investigation in oncogenic functions and immunological roles of NCBP2 and its validation in prostate cancer.Translational oncology · 2024Article
- The analysis of boric acid effect on epithelial-mesenchymal transition of CD133 + CD117 + lung cancer stem cells.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- The Many Roads from Alternative Splicing to Cancer: Molecular Mechanisms Involving Driver Genes.Cancers · 2024Review
- Article
- Review
- Ets family proteins regulate the EMT transcription factors Snail and ZEB in cancer cells.FEBS open bio · 2022Article
- Resident stroma-secreted chemokine CCL2 governs myeloid-derived suppressor cells in the tumor microenvironment.JCI insight · 2022Article
- Alternative RNA splicing in tumour heterogeneity, plasticity and therapy.Disease models & mechanisms · 2022Review
- Alternative splicing modulates cancer aggressiveness: role in EMT/metastasis and chemoresistance.Molecular biology reports · 2021Review
- Resveratrol and Its Analogs: Potent Agents to Reverse Epithelial-to-Mesenchymal Transition in Tumors.Frontiers in oncology · 2021Review
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial-mesenchymal transition (EMT) is a crucial morphological event that occurs during epithelial tumor progression. ZEB1/2 are EMT transcription factors that are positively correlated with EMT phenotypes and breast cancer aggressiveness. ZEB1/2 regulate the alternative splicing and hence isoform switching of fibroblast growth factor receptors (FGFRs) by repressing the epithelial splicing regulatory proteins, ESRP1 and ESRP2. Here, we show that the mesenchymal-like phenotypes of oral squamous cell carcinoma (OSCC) cells are dependent on autocrine FGF-FGFR signaling. Mesenchymal-like OSCC cells express low levels of ESRP1/2 and high levels of ZEB1/2, resulting in constitutive expression of the IIIc-isoform of FGFR, FGFR(IIIc). By contrast, epithelial-like OSCC cells showed opposite expression profiles for these proteins and constitutive expression of the IIIb-isoform of FGFR2, FGFR2(IIIb). Importantly, ERK1/2 was constitutively phosphorylated through FGFR1(IIIc), which was activated by factors secreted autonomously by mesenchymal-like OSCC cells and involved in sustained high-level expression of ZEB1. Antagonizing FGFR1 with either inhibitors or siRNAs considerably repressed ZEB1 expression and restored epithelial-like traits. Therefore, autocrine FGF-FGFR(IIIc) signaling appears to be responsible for sustaining ZEB1/2 at high levels and the EMT phenotype in OSCC cells.
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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.