ArticleClinical and translational medicine2022
Glioblastoma-educated mesenchymal stem-like cells promote glioblastoma infiltration via extracellular matrix remodelling in the tumour microenvironment.
Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 25 citations in OpenAlex.
- In Vivo CAR-Based Immune Cell Engineering: Future Applications and Challenges in Malignant Glioma.Cancers · 2026Review
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- Cellular Allies Against Glioblastoma: Therapeutic Potential of Macrophages and Mesenchymal Stromal Cells.Pharmaceutics · 2026Review
- The Extracellular Matrix, the Silent 'Architect' of Glioma.Biomedicines · 2026Review
- Ligand-receptor pair-based signature score derived from on-treatment tumor specimens predicts immune checkpoint blockade response in metastatic melanoma.Discover oncology · 2026Article
- Glioblastoma as a neuro-immune network disorder: rethinking the tumor microenvironment, neural circuit integration, and therapeutic resistance.Oncology reviews · 2026Review
- Restoring the glioblastoma tumor microenvironment by targeting C5a with the antagonist W54011.Scientific reports · 2025Article
- Article
- Machine learning derived development and validation of extracellular matrix related signature for predicting prognosis in adolescents and young adults glioma.Scientific reports · 2025Article
- Extracellular adenosine oppositely regulates the purinome machinery in glioblastoma and mesenchymal stem cells.IUBMB life · 2024Article
- Pathomics models for CD40LG expression and prognosis prediction in glioblastoma.Scientific reports · 2024Article
- Glucose metabolism in glioma: an emerging sight with ncRNAs.Cancer cell international · 2024Review
- HAS2 facilitates glioma cell malignancy and suppresses ferroptosis in an FZD7-dependent manner.Cancer science · 2024Article
- Article
- Revolutionizing Glioblastoma Treatment: A Comprehensive Overview of Modern Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Speeding up Glioblastoma Cancer Research: Highlighting the Zebrafish Xenograft Model.International journal of molecular sciences · 2024Review
- Glioblastoma-Associated Mesenchymal Stem/Stromal Cells and Cancer-Associated Fibroblasts: Partners in Crime?International journal of molecular sciences · 2024Review
- Identification of Hypoxia Prognostic Signature in Glioblastoma Multiforme Based on Bulk and Single-Cell RNA-Seq.Cancers · 2024Article
- Key Cell-in-Cell Related Genes are Identified by Bioinformatics and Experiments in Glioblastoma.Cancer management and research · 2024Article
- Article
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundThe biological function of mesenchymal stem-like cells (MSLCs), a type of stromal cells, in the regulation of the tumour microenvironment is unclear. Here, we investigated the molecular mechanisms underlying extracellular matrix (ECM) remodelling and crosstalk between MSLCs and glioblastomas (GBMs) in tumour progression.
methodsIn vitro and in vivo co-culture systems were used to analyze ECM remodelling and GBM infiltration. In addition, clinical databases, samples from patients with GBM and a xenografted mouse model of GBM were used.
resultsPrevious studies have shown that the survival of patients with GBM from whom MSLCs could be isolated is substantially shorter than that of patients from whom MSLCs could not be isolated. Therefore, we determined the correlation between changes in ECM-related gene expression in MSLC-isolatable patients with that in MSLC non-isolatable patients using gene set enrichment analysis (GSEA). We found that lysyl oxidase (LOX) and COL1A1 expressions increased in MSLCs via GBM-derived clusters of differentiation 40 ligand (CD40L). Mechanistically, MSLCs are reprogrammed by the CD40L/CD40/NFκB2 signalling axis to build a tumour infiltrative microenvironment involving collagen crosslinking. Importantly, blocking of CD40L by a neutralizing antibody-suppressed LOX expression and ECM remodelling, decreasing GBM infiltration in mouse xenograft models. Clinically, high expression of CD40L, clusters of differentiation 40 (CD40) and LOX correlated with poor survival in patients with glioma. This indicated that GBM-educated MSLCs promote GBM infiltration via ECM remodelling in the tumour microenvironment.
conclusionOur findings provide mechanistic insights into the pro-infiltrative tumour microenvironment produced by GBM-educated MSLCs and highlight a potential therapeutic target that can be used for suppressing GBM infiltration.
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