ArticleBiochemical and biophysical research communications2016
Senescence from glioma stem cell differentiation promotes tumor growth.
Article in Biochemical and biophysical research communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Reconstructing the molecular life history of gliomas.Acta neuropathologica · 2018Pooled it
- Article
- Primary glioma cell culture: from monolayer to organoids.Protoplasma · 2026Review
- Review
- Apoptotic and senolytic effects of hERG/Eag1 channel blockers in combination with temozolomide in human glioblastoma cells.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Nicotinamide metabolism reprogramming drives reversible senescence of glioblastoma cells.Cellular and molecular life sciences : CMLS · 2025Article
- Resistance to spindle inhibitors in glioblastoma depends on STAT3 and therapy induced senescence.iScience · 2024Article
- An untapped window of opportunity for glioma: targeting therapy-induced senescence prior to recurrence.NPJ precision oncology · 2023Review
- 5-Aminolevulinic acid increases boronophenylalanine uptake into glioma stem cells and may sensitize malignant glioma to boron neutron capture therapy.Scientific reports · 2023Article
- Adapt to Persist: Glioblastoma Microenvironment and Epigenetic Regulation on Cell Plasticity.Biology · 2022Review
- Modulation of BRCA1 mediated DNA damage repair by deregulated ER-α signaling in breast cancers.American journal of cancer research · 2022Article
- Role of Senescence in Tumorigenesis and Anticancer Therapy.Journal of oncology · 2022Review
- P4HA2 promotes cell proliferation and migration in glioblastoma.Oncology letters · 2021Article
- Glioblastoma Stem Cells: Driving Resilience through Chaos.Trends in cancer · 2020Review
- A way to understand idiopathic senescence and apoptosis in primary glioblastoma cells - possible approaches to circumvent these phenomena.BMC cancer · 2019Article
- Genomic evolution of cancer models: perils and opportunities.Nature reviews. Cancer · 2019Review
- PRMT5 as a druggable target for glioblastoma therapy.Neuro-oncology · 2018Article
- Effect of Necrosis on the miRNA-mRNA Regulatory Network in CRT-MG Human Astroglioma Cells.Cancer research and treatment · 2018Article
- Molecular subtypes and differentiation programmes of glioma stem cells as determinants of extracellular vesicle profiles and endothelial cell-stimulating activities.Journal of extracellular vesicles · 2018Article
- Development and optimization of an injectable formulation of copper diethyldithiocarbamate, an active anticancer agent.International journal of nanomedicine · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Glioblastoma (GBM) is a lethal brain tumor composed of heterogeneous cellular populations including glioma stem cells (GSCs) and differentiated non-stem glioma cells (NSGCs). While GSCs are involved in tumor initiation and propagation, NSGCs' role remains elusive. Here, we demonstrate that NSGCs undergo senescence and secrete pro-angiogenic proteins, boosting the GSC-derived tumor formation in vivo. We used a GSC model that maintains stemness in neurospheres, but loses the stemness and differentiates into NSGCs upon serum stimulation. These NSGCs downregulated telomerase, shortened telomeres, and eventually became senescent. The senescent NSGCs released pro-angiogenic proteins, including vascular endothelial growth factors and senescence-associated interleukins, such as IL-6 and IL-8. Conditioned medium from senescent NSGCs promoted proliferation of brain microvascular endothelial cells, and mixed implantation of GSCs and senescent NSGCs into mice enhanced the tumorigenic potential of GSCs. The senescent NSGCs seem to be clinically relevant, because both clinical samples and xenografts of GBM contained tumor cells that expressed the senescence markers. Our data suggest that senescent NSGCs promote malignant progression of GBM in part via paracrine effects of the secreted proteins.
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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.