ArticleScience advances2024
Cell-specific cross-talk proteomics reveals cathepsin B signaling as a driver of glioblastoma malignancy near the subventricular zone.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
10 citing papers in PubMed.
- CTSZ-dependent anoikis resistance enhances malignant characters of glioblastoma via NF-κB signaling.iScience · 2026Article
- The promising role of cathepsins as biomarkers and therapeutic targets in glioblastoma.Discover oncology · 2026Review
- Article
- Unveiling Anti-Cancer Potential through ADMET Prediction, Molecular Docking, Molecular Dynamics, andCurrent topics in medicinal chemistry · 2026Article
- Machine Learning Integration of Bulk and Single-Cell RNA-Seq Data Reveals Cathepsin B as a Central PANoptosis Regulator in Influenza.International journal of molecular sciences · 2025Article
- TurboID-Mediated Profiling of Glioblastoma-Derived Extracellular Vesicle Cargo Proteins.Journal of extracellular vesicles · 2025Article
- Integration of multi-omics approaches in exploring intra-tumoral heterogeneity.Cancer cell international · 2025Review
- Platinum(IV) anticancer therapies and cathepsin B: innovative strategies for overcoming resistance in glioblastoma cells.Frontiers in cell and developmental biology · 2025Article
- Human Melanoma and Glioblastoma Cells Express Cathepsins Supporting Reovirus Moscow Strain Infection.Viruses · 2024Article
- [Glioblastoma and its interaction with neurogenesis].Revista de neurologia · 2024Review
Corrections and comments
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18 authors.
Funding
Abstract
Glioblastoma (GBM) is the most prevalent and aggressive malignant primary brain tumor. GBM proximal to the lateral ventricles (LVs) is more aggressive, potentially because of subventricular zone contact. Despite this, cross-talk between GBM and neural stem/progenitor cells (NSC/NPCs) is not well understood. Using cell-specific proteomics, we show that LV-proximal GBM prevents neuronal maturation of NSCs through induction of senescence. In addition, GBM brain tumor-initiating cells (BTICs) increase expression of cathepsin B (CTSB) upon interaction with NPCs. Lentiviral knockdown and recombinant protein experiments reveal that both cell-intrinsic and soluble CTSB promote malignancy-associated phenotypes in BTICs. Soluble CTSB stalls neuronal maturation in NPCs while promoting senescence, providing a link between LV-tumor proximity and neurogenesis disruption. Last, we show LV-proximal CTSB up-regulation in patients, showing the relevance of this cross-talk in human GBM biology. These results demonstrate the value of proteomic analysis in tumor microenvironment research and provide direction for new therapeutic strategies in GBM.
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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 Socratic graph.