ArticleCancer science2026
TGM2 Regulates Radiosensitivity via POGZ-Mediated Repair of DNA Double-Strand Breaks in Cervical Cancer.
Article in Cancer science, 2026. 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.
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Who cites it
3 citing papers in PubMed.
- A three-gene radioresistance signature predicts tumor progression in cervical cancer.Translational cancer research · 2026Article
- OV16 Improves Radiation-Induced Intestinal Injury by Targeting Transglutaminase 2.Molecules (Basel, Switzerland) · 2026Article
- Inhibition of TGM2 enhances cisplatin sensitivity in MSH2-deficient bladder cancer.Cell death discovery · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The high capacity of cancer cells for DNA damage repair constitutes a critical factor contributing to their radioresistance. Previous studies have demonstrated that aberrant expression of transglutaminase 2 (TGM2) is linked to treatment resistance. However, the role of TGM2 in cervical cancer radiosensitivity and its underlying mechanisms remain unclear. In this study, we found that TGM2 was significantly upregulated in radioresistant cervical cancer cells and tissues. TGM2 knockdown significantly enhanced the radiosensitivity of cervical cancer cells, while TGM2 overexpression conferred radioresistance. TGM2 depletion exacerbated ionizing radiation (IR)-induced DNA double-strand breaks (DSBs). Mechanistically, IR triggered the nuclear translocation of TGM2, where it physically interacted with POGO transposable element derived with ZNF domain protein (POGZ) and upregulated POGZ protein levels. TGM2 knockdown impaired BRCA1 recruitment to DSB sites, phenocopying POGZ depletion effects. Rescue experiments demonstrated that POGZ knockdown reversed the radioresistance and reduction in DNA DSBs caused by TGM2 overexpression. Subcutaneous xenograft mouse models further verified these findings and the regulatory role of TGM2 in cervical cancer radiosensitivity in vivo. Together, our results demonstrated that TGM2 regulates radiosensitivity by POGZ-mediated DNA DSBs repair, providing a novel strategy for increasing cervical cancer radiosensitivity.
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Registered trials
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