ArticleCancer cell international2025
STAT3/TGFBI signaling promotes the temozolomide resistance of glioblastoma through upregulating glycolysis by inducing cellular senescence.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed.
- An EGFR-Targeted Fusogenic Tandem Peptide for siRNA Delivery in Glioblastoma.Pharmaceutics · 2026Article
- Article
- Review
- NF-κB and STAT3 signaling uniquely stratify survival in female glioblastoma patients.iScience · 2026Article
- Review
- TGFBI in tumors and the tumor immune microenvironment: functional roles, mechanisms, and therapeutic targeting.Frontiers in immunology · 2026Review
- Progress in the study of molecular markers in the prognosis assessment and recurrence patterns of glioblastoma.Cancer biology & therapy · 2025Review
- Histone demethylase KDM4C confers temozolomide resistance to glioblastoma cells by epigenetically regulating E2F6.Archives of pharmacal research · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Glioblastoma (GBM) is the most lethal type of brain tumor. Recent studies have indicated that cellular senescence-targeted therapy is a promising approach for cancer treatment. However, the underlying mechanisms remain to be clarified. In this study, 101 unique combinations of 10 machine learning algorithms were used to construct prognostic models based on cellular senescence-related genes (CSRGs). We developed the CSRG signature (CSRGS) using machine learning models that exhibited optimal performance. GBM samples were stratified into high- and low-CSRGS groups based on CSRGS scores. Patients in the high-CSRGS group exhibited a worse prognosis, higher immune infiltration, and increased sensitivity to immune checkpoint blockade therapy. Furthermore, senescence-related pathways were significantly correlated with glycolysis, indicating upregulated glycolytic metabolism in senescent GBM cells. We identified TGFBI as a key regulator that played vital roles in both glycolysis and cellular senescence in GBM. TGFBI was overexpressed in GBM samples compared to normal brain tissues, and its knockdown via shRNA inhibited cellular senescence, glycolysis, and temozolomide resistance. Chromatin immunoprecipitation (ChIP) and luciferase reporter assays confirmed that TGFBI is a direct STAT3 target and is required for the STAT3-induced promotion of cellular senescence, glycolysis, and drug resistance. The STAT3-TGFBI axis could be a potential target for senescence-targeted GBM therapy.
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Registered trials
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