ArticleJournal of cell science2026
Cancer metabolism in radiation sensitization - complementary roles of O-GlcNAc transferase and PARP1.
Article in Journal of cell science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Glutamine metabolism and its roles in tumor radiotherapy by regulating DNA damage repair.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
For double-strand breaks (DSBs) formed by radiation, the onset of 5' to 3' end resection is a deciding factor in repair pathway choice, favoring homologous recombination (HR) over non-homologous end-joining (NHEJ). Studying HR-proficient MCF7 breast cancer cells, we confirmed a role for PARP1 in promoting DSB repair and limiting resection stress and identified the hexosamine biosynthetic pathway (HBP)-dependent post-translational modification O-GlcNAcylation as an independent regulator. Using pharmacological and genetic perturbations of O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT) and O-GlcNAcase (OGA), we showed that O-GlcNAcylation can limit end resection as measured by BrdU and RPA staining, recruitment of HR proteins BRCA1 and RAD51, and accumulation of cytosolic DNA in S/G2-phase cells. These effects were independent of PARP1 but required the histone methyltransferase EZH2. Loss of OGT or EZH2 phenocopied PARP inhibition, leading to hyper-resection after irradiation. The OGA inhibitor PUGNAc suppressed hyper-resection due to PARP1 knockout whereas treatment with the PARP inhibitor veliparib exacerbated defects in OGT- or EZH2-deficient cells. In each case, increased resection correlated with cytosolic DNA accumulation, suggesting a link to inflammatory signaling. These findings implicate the Warburg effect, via the HBP and O-GlcNAcylation, in favoring NHEJ over HR and suggest that disrupting EZH2 may sensitize HR-proficient tumor cells to radiation via resection-dependent mechanisms. Our results highlight the potential of targeting cancer-associated metabolic reprogramming to overwhelm HR repair and drive resection stress. Combining PARP inhibition with blockade of O-GlcNAcylation or EZH2 might offer a strategy to radiosensitize proliferating HR-proficient cancers while sparing non-cycling normal tissues.
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Registered trials
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