ArticleCell death & disease2025
Temozolomide promotes glioblastoma stemness expression through senescence-associated reprogramming via HIF1α/HIF2α regulation.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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.
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Who cites it
27 citing papers in PubMed.
- Stem-like characteristics across sequentially temozolomide-adapted glioblastoma cell populations with increasing levels of acquired resistance.Molecular biology reports · 2026Article
- Characterizing the SASP-Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types.Aging cell · 2026Article
- Temozolomide and ruxolitinib combination modulates miRNA-associated regulatory networks in glioblastoma stem cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- HIFs: The central drivers of tumors and their role as molecular switches in targeted therapy?Acta pharmaceutica Sinica. B · 2026Review
- CD13 identifies S100A4Biology direct · 2026Article
- Fate Bifurcation of Cellular Senescence: Dynamic Regulation from Tumor Suppression to Recurrence Risk.Cells · 2026Review
- Cryogenic Electron Microscopy of Extracellular Vesicles from Temozolomide-Treated Glioblastoma Cells Reveals Great Morphological Heterogeneity.Nanomaterials (Basel, Switzerland) · 2026Article
- Advanced drug delivery platforms targeting cellular senescence: A promising strategy for cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- Integrated biomarker mapping reveals differential expression of senescence profiles in IDH-wild-type glioblastoma recurrent versus primary tumors.Virchows Archiv : an international journal of pathology · 2026Article
- The Size of Glioblastoma Spheroids Influences Patterns of Invasion and Temozolomide Efficacy.Tissue engineering. Part C, Methods · 2026Article
- Open micro-valley chip reveals long-term viscosity-induced glioblastoma cellular invasion states.Microsystems & nanoengineering · 2026Article
- SLC25A1 upregulation promotes HNSCC cisplatin resistance via H3K27ac-mediated cellular senescence.NPJ precision oncology · 2026Article
- Review
- YBX1 promotes angiogenesis after myocardial infarction by stabilizing HIF1α mRNA via miScience · 2026Article
- Overcoming Chemoresistance in Glioblastoma: Mechanisms, Therapeutic Strategies, and Functional Precision Medicine.International journal of molecular sciences · 2026Review
- Distinct molecular pathways leading to dosage-dependent temozolomide resistance in GBM stem cells.Cancer cell international · 2026Article
- Review
- Review
- Coupling proteostasis andTheranostics · 2026Article
- Correlative study ofFrontiers in microbiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
A critical challenge in glioblastoma multiforme (GBM) treatment is that tumors recurring after temozolomide (TMZ) therapy become more malignant, exhibiting increased invasiveness and stemness compared to the primary tumor. However, the underlying mechanisms remain unclear. While the majority of GBM cells are eradicated by TMZ, a subset enters cell cycle arrest, adopts a senescence-associated secretory phenotype (SASP), and activates senescence-related signaling pathways. These cells eventually escape senescence, re-enter the cell cycle, and form aggregates exhibiting stem-like characteristics such as elevated stemness marker expression, enhanced colony formation, increased invasiveness, and resistance to chemotherapy. Furthermore, these aggregates promote the invasion and chemotherapy resistance of surrounding cells. Gene Set Enrichment Analysis (GSEA) and KEGG pathway analysis of miRNA and mRNA sequences revealed activation of hallmark hypoxia and HIF1 signaling pathways. The study demonstrated that HIF1α and HIF2α expression fluctuates during and after TMZ treatment. Knockout of HIF1α and HIF2α in GBM cells exposed to TMZ reduced the formation of senescent cells and stem-like aggregates. These findings challenge the efficacy of TMZ therapy by highlighting its role in inducing the process of cellular senescence, thereby contributing to the enhanced stemness and malignancy of recurrent GBM. The regulatory roles of HIF1α and HIF2α are emphasized, underscoring the necessity of preventing senescent cell formation and inhibiting HIF1α/HIF2α expression to improve therapeutic outcomes.
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