ArticleScientific reports2025
RUNX2 mediated epithelial mesenchymal transition induced by TGF beta and Smad signaling promotes malignant progression in glioma.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Article
- FCGBP promotes malignant phenotypes of glioblastoma cells via activation of the TGF-β1 signaling pathway.American journal of translational research · 2026Article
- Research Progress on Signaling Pathways in Breast Cancer Bone Metastasis.Oncology research · 2026Review
- Single-cell analysis identifies a VIM+ glioma stem-like vascular-immune state linked to myeloid OSM signaling and CEBPD activity.Frontiers in immunology · 2026Article
- Epigenetic Regulation of RUNX2 in Bone Mechanobiology.Results and problems in cell differentiation · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
RUNX2, a member of the RUNX transcription factor family, has been reported to promote epithelial-mesenchymal transition (EMT) in various malignancies, yet its role in glioma remains poorly understood. In this study, we systematically analyzed RUNX2 expression and clinical relevance in glioma using The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) datasets via the UALCAN web portal. Kaplan-Meier survival analyses and Wilcoxon rank-sum tests were employed to assess the prognostic significance of RUNX2. We further validated RUNX2 expression in glioma tissues and cell lines using RT-qPCR and Western blotting. Functional experiments, including CCK-8, wound healing, transwell invasion, and apoptosis assays, were conducted in U251 glioma cells with RUNX2 knockdown via siRNA. EMT-related proteins and components of the TGF-β/Smad pathway were examined by Western blot. In addition, we employed multiplex immunohistochemistry on 160 glioma specimens to analyze the spatial relationship between RUNX2 and EMT markers. Our results demonstrate that RUNX2 is significantly upregulated in glioma tissues and correlates with higher tumor grade, IDH-wildtype status, and poorer overall and disease-free survival. RUNX2 knockdown significantly inhibited glioma cell proliferation, migration, and invasion, while promoting apoptosis. Mechanistically, RUNX2 modulated the expression of EMT markers and activated the TGF-β1/Smad2/3 signaling axis. Collectively, our findings suggest that RUNX2 promotes EMT and malignant progression in glioma via the TGF-β/Smad pathway, and may serve as a potential therapeutic target and prognostic biomarker.
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