ArticleNature communications2025
Endothelial-secreted Endocan activates PDGFRA and regulates vascularity and spatial phenotype in glioblastoma.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed.
- Engineered Microvascular Model of the Blood-Brain-Tumor Barrier Reveals Endothelial Remodeling in Diffuse Midline Glioma.Advanced healthcare materials · 2026Article
- Anti-PDGFRα autoantibody - a novel diagnostic and prognostic marker - may mediate non-small cell lung cancer progression via the PI3K/AKT/NF-κB signaling pathway.British journal of cancer · 2026Article
- Integrative transcriptomic, spatial and functional-genomic analysis identifies a UFMylation-related vascular-stromal program and prioritizes WWTR1 in glioblastoma.Functional & integrative genomics · 2026Article
- The Invasive Margin of Glioblastoma as a Molecular Ecosystem: Spatial Heterogeneity, Tumor-Host Interactions, and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Spatial Omics Technologies in Glioblastoma Research: Principles, Applications, and Best Practices.Genes · 2026Review
- Role of NR2F2-mediated reprogramming of endothelial cells in glioblastoma progression.iScience · 2026Article
- Disrupting MED8-dependent epigenetic reprogramming augments avapritinib sensitivity in PDGFRA-driven glioma.Journal of experimental & clinical cancer research : CR · 2026Article
- LSD1-ESM1 regulates extravillous trophoblast function through metabolic reprogramming in recurrent spontaneous abortion.Journal of assisted reproduction and genetics · 2026Article
- Prognostic Role of Endocan and Platelet-Derived Growth Factor Isoforms in Metastatic Colorectal Cancer.International journal of molecular sciences · 2026Article
- Chromatin Accessibility in Cancer: Biological Functions, Mechanisms, Therapeutic Potential, and Future Directions.MedComm · 2026Review
- Dysregulation of post-translational modifications in glioma: advances in pathological mechanisms and clinical targeting strategies.Journal of translational medicine · 2026Review
- Disrupting PDGFRA-driven immune evasion in glioma: vaccine-based strategies on the horizon.Frontiers in oncology · 2026Review
- Development of a comparative high-throughput screening platform for identifying glioblastoma subtype specific inhibitors.Cell insight · 2025Article
- Current evidence and challenges of multitarget anti-angiogenic agents for glioblastoma: Results from clinical trials.iScience · 2025Review
- Crosstalk between tumor endothelial cells and cancer cells is important for metastasis initiation.Cell communication and signaling : CCS · 2025Article
- Dermatan Sulfate: Structure, Biosynthesis, and Biological Roles.Biomolecules · 2025Review
- Bevacizumab‑associated intracerebral hemorrhage in patients with malignant glioma.Molecular and clinical oncology · 2025Article
Corrections and comments
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Authors and funding
26 authors.
Funding
Abstract
Extensive neovascularization is a hallmark of glioblastoma (GBM). In addition to supplying oxygen and nutrients, vascular endothelial cells provide trophic support to GBM cells via paracrine signaling. Here we report that Endocan (ESM1), an endothelial-secreted proteoglycan, confers enhanced proliferative, migratory, and angiogenic properties to GBM cells and regulates their spatial identity. Mechanistically, Endocan exerts at least part of its functions via direct binding and activation of the PDGFRA receptor. Subsequent downstream signaling enhances chromatin accessibility of the Myc promoter and upregulates Myc expression inducing stable phenotypic changes in GBM cells. Furthermore, Endocan confers radioprotection on GBM cells in vitro and in vivo. Inhibition of Endocan-PDGFRA signaling with ponatinib increases survival in the Esm1 wild-type but not in the Esm1 knock-out mouse GBM model. Our findings identify Endocan and its downstream signaling axis as a potential target to subdue GBM recurrence and highlight the importance of vascular-tumor interactions for GBM development.
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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.