ArticleJournal of neuro-oncology2025
Targeting ataxia-telangiectasia mutated and cystine/glutamate antiporter enhances radiotherapy efficacy and tumor suppression in glioblastoma.
Article in Journal of neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- FLASH Radiotherapy and Organelle-Targeted Radiosensitization in Glioblastoma: A Conceptual and Translational Review.Cancers · 2026Review
- Beyond Epilepsy Control: Repurposing Antiepileptic Drugs in Central Nervous System Tumor Therapy.Cells · 2026Review
- Ferroptosis and metastasis: molecular checkpoints, microenvironmental dynamics, and therapeutic opportunities.Molecular cancer · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeGlioblastoma (GBM) is the most common and lethal primary brain tumor in adults, with a dismal prognosis owing to its intrinsic radioresistance. Overcoming radioresistance is crucial to improving radiotherapy efficacy; however, effective strategies remain elusive. The ataxia-telangiectasia mutated (ATM) protein, a central regulator of the DNA damage response, is crucial in repairing irradiation-induced DNA double-strand breaks (DSBs), contributing to radioresistance in GBM. The cystine/glutamate antiporter xCT, which is overexpressed in GBM, also maintains intracellular redox balance by promoting glutathione synthesis, enhancing tumor survival under oxidative stress.
methodsIn this study, we hypothesized that the simultaneous inhibition of ATM and cystine/glutamate antiporter (xCT; SLC7A11) would enhance radiosensitivity by impairing DSB repair and redox homeostasis. We performed clonogenic assays and immunofluorescence staining of phospho-γ-H2AX, a marker of radiation-induced DNA DSBs, to evaluate the in vitro efficacy of radiosensitivity of glioma cell lines. To investigate the in vivo effects of simultaneous ATM and xCT inhibition, we observed tumor radiosensitivity in an established mouse model using brain-specific irradiation combined with dual inhibition of ATM and xCT.
resultsSimultaneous inhibition of ATM and xCT significantly decreased colony formation in glioma cells beyond the effect of irradiation. Additionally, phosphorylated γ-H2AX immunofluorescence staining confirmed that DNA double-strand break (DSB) induction was greater with the combination therapy than with radiation alone. Simultaneous inhibition of either ATM or xCT enhanced radiosensitivity and reduced tumor growth compared to irradiation alone in vivo.
conclusionIn in vitro and in vivo GBM models, the simultaneous inhibition of ATM and xCT significantly increased radiosensitivity, reduced tumor cell viability, and suppressed tumor growth. These findings highlight a promising dual-targeting strategy for overcoming GBM radioresistance and improving radiotherapy outcomes.
Indexed as
Identifiers
40676327What Socratic holds
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.