ArticleScientific reports2025
Expression of DNA-damage response genes after exposure to high LET particles used in BNCT in glioblastoma cells with altered radiosensitivity.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- BKJournal of neuro-oncology · 2026Article
- NCOA4 as a regulatory switch linking DNA damage to lipid peroxidation in radiation response.Frontiers in cell and developmental biology · 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
16 authors.
Funding
Abstract
DNA-dependent protein kinase catalytic subunit (DNA-PKcs) plays a central role in the repair of double-strand breaks (DSBs), but its deficiency alters the broader DNA damage response in glioblastoma cells exposed to α particle irradiation. Here, we investigated transcriptional changes in DNA repair pathways and cellular radiosensitivity in two isogenic glioblastoma cell lines differing in DNA-PKcs status: M059J (DNA-PKcs-deficient) and M059K (DNA-PKcs-proficient). Using pathway-focused qPCR, we profiled 30 genes involved in key DNA repair pathways and evaluated cell survival by clonogenic and MTT assays. M059J cells, despite DNA-PKcs deficiency, exhibited comparable survival fractions and higher metabolic activity than DNA-PKcs-proficient M059K cells following α particle irradiation. Irradiated M059J cells exhibited broad transcriptional upregulation of genes involved in double-strand break repair, single-strand break repair, mismatch repair, and nucleotide excision repair, reflecting compensatory activation of multiple repair mechanisms. In contrast, M059K cells displayed a restricted response, characterized primarily by strong PRKDC upregulation, the gene encoding DNA-PKcs. These findings highlight the pivotal role of DNA-PKcs status in shaping the DNA damage response and radiosensitivity of glioblastoma cells. Targeting compensatory repair pathways in DNA-PKcs-deficient tumors may offer novel strategies for radiosensitization in glioblastoma therapy.
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