ArticleCancer biology & therapy2020
Glutamine synthetase facilitates cancer cells to recover from irradiation-induced G2/M arrest.
Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Oncogene c‑Myc: From molecular mechanism to targeted therapy (Review).Molecular medicine reports · 2026Review
- A different perspective on the cancer stem cell theory.Medical oncology (Northwood, London, England) · 2026Review
- MTHFD2 is required for DNA repair and implicated in LUAD radiotherapy resistance.Journal of translational medicine · 2026Article
- The regulatory role and mechanism of energy metabolism and immune response in head and neck cancer.Genes & diseases · 2025Review
- Inhibition of glutamine synthetase enhances hepatocellular carcinoma radiosensitivity through ROS-induced excessive mitophagy.Molecular biology reports · 2025Article
- The Dose Rate of Corpuscular Ionizing Radiation Strongly Influences the Severity of DNA Damage, Cell Cycle Progression and Cellular Senescence in Human Epidermoid Carcinoma Cells.Current issues in molecular biology · 2024Article
- CDC25B Is a Prognostic Biomarker Associated With Immune Infiltration and Drug Sensitivity in Hepatocellular Carcinoma.International journal of genomics · 2024Article
- Glutamine regulates the cellular proliferation and cell cycle progression by modulating the mTOR mediated protein levels of β-TrCP.Cell cycle (Georgetown, Tex.) · 2023Article
- Article
- Novel insight into metabolic reprogrammming in cancer radioresistance: A promising therapeutic target in radiotherapy.International journal of biological sciences · 2023Review
- Mechanism-Based Sonodynamic-Chemo Combinations against Triple-Negative Breast Cancer.International journal of molecular sciences · 2022Article
- Overcoming Radiation Resistance in Gliomas by Targeting Metabolism and DNA Repair Pathways.International journal of molecular sciences · 2022Review
- Glutamine Synthetase as a Therapeutic Target for Cancer Treatment.International journal of molecular sciences · 2021Review
- Metabolic Reprogramming and Immune Evasion in Nasopharyngeal Carcinoma.Frontiers in immunology · 2021Review
- DNA damage response signaling pathways and targets for radiotherapy sensitization in cancer.Signal transduction and targeted therapy · 2020Review
- Metabolic pathways underlying GATA6 regulating Trastuzumab resistance in Gastric Cancer cells based on untargeted metabolomics.International journal of medical sciences · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to radiation of cancer cells can be either intrinsic or acquired, leading to treatment failure. In response to DNA damage caused by IR, cancer cells are arrested in cell cycle showing limited proliferation and increased apoptosis. However, radiation-resistant cells are able to overcome the cell cycle block and proceed to proliferation, for which the detailed mechanism remains to be elucidated. In the present study, we showed that radioresistant cells exhibited a recoverable G2/M phase during prolonged cell cycle and manifested lower apoptosis rate and more colony formation. RNA-seq analysis revealed that glutamine synthetase (GS, GLUL) gene was highly expressed in radioresistant cancer cells in comparison with the parental cells, which was in accordance with the G2/M arrest after ionizing radiation. Knocking out of GS in radioresistant cells resulted in a delayed G2/M recovery and lowered proliferation rate after ionizing radiation treatment, which was accompanied with increased inhibitory phosphorylation of CDK1 at Y15 and downregulated Cdc25B, a dual specific phosphatase of CDK1. Moreover, there was an enhanced complex formation of CDK1 and Cyclin B1 when the cells were rescued by re-introducing GS. In vivo, knocking down of GS significantly sensitized CNE2-R xenografts to RT in mice. In this study, we demonstrate a novel role of glutamine synthetase independent of metabolic function in promoting recovery from G2/M arrest caused by ionizing radiation, thus, causing cancer cell resistance to radiotherapy.
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