ArticleEBioMedicine2019
Gene signatures of quiescent glioblastoma cells reveal mesenchymal shift and interactions with niche microenvironment.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed.
- CRISPR/Cas9 Genome Editing in Oncology: Mechanisms, Therapeutic Platforms and Translational Challenges.Molecular biotechnology · 2026Review
- The lysine methyltransferase KMT5a and p53 regulate the expression of the key autophagy adaptor p62/SQSTM1 in glioblastoma.Cell communication and signaling : CCS · 2026Article
- Engineered nanomedicine remodels the postoperative cavity microenvironment to suppress glioblastoma recurrence.Theranostics · 2026Review
- CEBPB-high dormant tumor cells drive immune evasion via S100A8 orchestrated tumor-associated macrophages reprogramming.Theranostics · 2026Article
- Glioblastoma shift from bulk to infiltrative growth is guided by plexin-B2-mediated microglia alignment in invasive niches.Nature cancer · 2025Article
- 3D Brain Vascular Niche Model Captures Glioblastoma Infiltration, Dormancy, and Gene Signatures.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integrating multi-omics data to identify the role of Aggrephagy-related genes in tumor microenvironment and key tumorigenesis factors of GB from the perspective of single-cell sequencing.Discover oncology · 2025Article
- p21-Dependent Senescence Induction by BMP4 Renders Glioblastoma Cells Vulnerable to Senolytics.International journal of molecular sciences · 2025Article
- CutIn: a ready-to-use construct for rapid generation of urgently needed transgenic cell lines in emerging infection research.Functional & integrative genomics · 2025Article
- Classifying cell cycle states and a quiescent-like G0 state using single-cell transcriptomics.bioRxiv : the preprint server for biology · 2025Article
- Invasion of glioma cells through confined space requires membrane tension regulation and mechano-electrical coupling via Plexin-B2.Nature communications · 2025Article
- Niche-specific epigenetic interventions in the spatially heterogeneous glioblastoma microenvironmental landscape: strategies for radiotherapy enhancement.Frontiers in molecular biosciences · 2025Review
- A New Perspective on Precision Medicine: The Power of Digital Organoids.Biomaterials research · 2025Review
- Brain Tumor Stem Cells: New Perspectives.Methods in molecular biology (Clifton, N.J.) · 2025Review
- Resistance to spindle inhibitors in glioblastoma depends on STAT3 and therapy induced senescence.iScience · 2024Article
- The neglected burden of chronic hypoxia on the resistance of glioblastoma multiforme to first-line therapies.BMC biology · 2024Review
- Review
- Preclinical and clinical advances to overcome hypoxia in glioblastoma multiforme.Cell death & disease · 2024Review
- Review
- Understanding the immunosuppressive microenvironment of glioma: mechanistic insights and clinical perspectives.Journal of hematology & oncology · 2024Review
20 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors.
Funding
Abstract
backgroundGlioblastoma (GBM), a highly malignant brain tumor, invariably recurs after therapy. Quiescent GBM cells represent a potential source of tumor recurrence, but little is known about their molecular underpinnings.
methodsPatient-derived GBM cells were engineered by CRISPR/Cas9-assisted knock-in of an inducible histone2B-GFP (iH2B-GFP) reporter to track cell division history. We utilized an in vitro 3D GBM organoid approach to isolate live quiescent GBM (qGBM) cells and their proliferative counterparts (pGBM) to compare stem cell properties and therapy resistance. Gene expression programs of qGBM and pGBM cells were analyzed by RNA-Seq and NanoString platforms.
findingsH2B-GFP-retaining qGBM cells exhibited comparable self-renewal capacity but higher therapy resistance relative to pGBM. Quiescent GBM cells expressed distinct gene programs that affect cell cycle control, metabolic adaptation, and extracellular matrix (ECM) interactions. Transcriptome analysis also revealed a mesenchymal shift in qGBM cells of both proneural and mesenchymal GBM subtypes. Bioinformatic analyses and functional assays in GBM organoids established hypoxia and TGFβ signaling as potential niche factors that promote quiescence in GBM. Finally, network co-expression analysis of TCGA glioma patient data identified gene modules that are enriched for qGBM signatures and also associated with survival rate.
interpretationOur in vitro study in 3D GBM organoids supports the presence of a quiescent cell population that displays self-renewal capacity, high therapy resistance, and mesenchymal gene signatures. It also sheds light on how GBM cells may acquire and maintain quiescence through ECM organization and interaction with niche factors such as TGFβ and hypoxia. Our findings provide a starting point for developing strategies to tackle the quiescent population of GBM. FUND: National Institutes of Health (NIH) and Deutsche Forschungsgemeinschaft (DFG).
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