ArticleMolecular cancer2010
TWIST1 promotes invasion through mesenchymal change in human glioblastoma.
Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 2 of them syntheses that pooled it.
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Who cites it
188 citing papers in PubMed, 2 syntheses or guidelines pooled it, 293 citations in OpenAlex.
- Systematic review of protein biomarkers of invasive behavior in glioblastoma.Molecular neurobiology · 2014Pooled it
- A systematic review of microRNA in glioblastoma multiforme: micro-modulators in the mesenchymal mode of migration and invasion.Molecular neurobiology · 2013Pooled it
- The critical role of the endogenous immune compartment after CAR T cell therapy in recurrent GBM.Cell · 2026Article
- Mesenchymal transitions reduce lamin A expression and nuclear stiffness to enhance confined migration in glioblastoma.Scientific reports · 2026Article
- Single-cell and bulk transcriptome analysis reveals the impact of inflammatory microglia on prognosis and immunotherapy response in primary glioblastoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- SDK1 as an Independent Prognostic Biomarker in Primary Glioma: A Multi-Cohort Validation Study with Functional Characterization.International journal of molecular sciences · 2026Article
- Identification of biomarkers associated with integrated stress response in pituitary adenomas based on bioinformatics.Discover oncology · 2026Article
- Overcoming Chemoresistance in Glioblastoma: Mechanisms, Therapeutic Strategies, and Functional Precision Medicine.International journal of molecular sciences · 2026Review
- From bench to bedside, blade, and back: FAP expression in juvenile angiofibroma. Potential implications for FAPI-PET/CT imaging and targeted therapy?European journal of nuclear medicine and molecular imaging · 2026Article
- The significance of epithelial-mesenchymal transition (EMT) in the initiation, plasticity, and treatment of glioblastoma.Genes & diseases · 2026Review
- Comparison of the Effect of the Combination of Sodium Valproate and Sodium Dichloroacetate on the Expression ofPharmaceutics · 2025Article
- Epithelial-Mesenchymal Transition and Genetically Driven Early Tumor Seedings in Extraneural Metastasis of Glioblastoma.Cancer science · 2025Article
- Article
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- Effects ofMarine drugs · 2025Article
- Dual nuclear receptor 4A1 (NR4A1/NR4A2) ligands inhibit glioblastoma growth and target TWIST1.Molecular pharmacology · 2025Article
- Hypoxia Dependent Inhibition of Glioblastoma Cell Proliferation, Invasion, and Metabolism by the Choline-Kinase Inhibitor JAS239.Metabolites · 2025Article
- GADD45G as a novel prognostic biomarker and therapeutic target in glioma: integrative analysis of bulk and single-cell RNA sequencing.Frontiers in oncology · 2025Article
- Fibrillar extracellular matrix produced by pericyte-like cells facilitates glioma cell dissemination.Brain pathology (Zurich, Switzerland) · 2024Article
- Increased FGL1 Expression Predicts Poor Prognosis and Promotes EMT in Head and Neck Squamous Cell Carcinoma.Biochemical genetics · 2024Article
128 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
Abstract
backgroundTumor cell invasion into adjacent normal brain is a mesenchymal feature of GBM and a major factor contributing to their dismal outcomes. Therefore, better understandings of mechanisms that promote mesenchymal change in GBM are of great clinical importance to address invasion. We previously showed that the bHLH transcription factor TWIST1 which orchestrates carcinoma metastasis through an epithelial mesenchymal transition (EMT) is upregulated in GBM and promotes invasion of the SF767 GBM cell line in vitro.
resultsTo further define TWIST1 functions in GBM we tested the impact of TWIST1 over-expression on invasion in vivo and its impact on gene expression. We found that TWIST1 significantly increased SNB19 and T98G cell line invasion in orthotopic xenotransplants and increased expression of genes in functional categories associated with adhesion, extracellular matrix proteins, cell motility and locomotion, cell migration and actin cytoskeleton organization. Consistent with this TWIST1 reduced cell aggregation, promoted actin cytoskeletal re-organization and enhanced migration and adhesion to fibronectin substrates. Individual genes upregulated by TWIST1 known to promote EMT and/or GBM invasion included SNAI2, MMP2, HGF, FAP and FN1. Distinct from carcinoma EMT, TWIST1 did not generate an E- to N-cadherin "switch" in GBM cell lines. The clinical relevance of putative TWIST target genes SNAI2 and fibroblast activation protein alpha (FAP) identified in vitro was confirmed by their highly correlated expression with TWIST1 in 39 human tumors. The potential therapeutic importance of inhibiting TWIST1 was also shown through a decrease in cell invasion in vitro and growth of GBM stem cells.
conclusionsTogether these studies demonstrated that TWIST1 enhances GBM invasion in concert with mesenchymal change not involving the canonical cadherin switch of carcinoma EMT. Given the recent recognition that mesenchymal change in GBMs is associated with increased malignancy, these findings support the potential therapeutic importance of strategies to subvert TWIST1-mediated mesenchymal change.
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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.