ArticleInternational journal of oncology2018
Nuclear GSK3β induces DNA double-strand break repair by phosphorylating 53BP1 in glioblastoma.
Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Links between the unfolded protein response and the DNA damage response in hypoxia: a systematic review.Biochemical Society transactions · 2021Pooled it
- GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1.The Journal of clinical investigation · 2025Article
- Loss of genome maintenance is linked to mTOR complex 1 signaling and accelerates podocyte damage.JCI insight · 2025Article
- Inhibition of GSK3β is synthetic lethal with FHIT loss in lung cancer by blocking homologous recombination repair.Experimental & molecular medicine · 2025Article
- Construction of a novel lipid drop-mitochondria-associated genetic profile for predicting the survival and prognosis of lung adenocarcinoma.Discover oncology · 2024Article
- Integrating Machine Learning and Mendelian Randomization Determined a Functional Neurotrophin-Related Gene Signature in Patients with Lower-Grade Glioma.Molecular biotechnology · 2024Article
- Tau beyond Tangles: DNA Damage Response and Cytoskeletal Protein Crosstalk on Neurodegeneration.International journal of molecular sciences · 2024Review
- IQGAP3 promotes the progression of glioma as an immune and prognostic marker.Oncology research · 2024Article
- Symmetric control of sister chromatid cohesion establishment.Nucleic acids research · 2023Article
- Crosstalk between Wnt/β-catenin signaling pathway and DNA damage response in cancer: a new direction for overcoming therapy resistance.Frontiers in pharmacology · 2023Review
- The DNA Double-Strand Break Repair in Glioma: Molecular Players and Therapeutic Strategies.Molecular neurobiology · 2022Review
- Multifaceted regulation and functions of 53BP1 in NHEJ‑mediated DSB repair (Review).International journal of molecular medicine · 2022Review
- Decrypting a path based approach for identifying the interplay between PI3K and GSK3 signaling cascade from the perspective of cancer.Genes & diseases · 2022Review
- Construction and Validation of a Necroptosis-Related Gene Signature for Predicting Prognosis and Tumor Microenvironment of Pancreatic Cancer.Disease markers · 2022Article
- Molecular mechanisms of ferroptosis and the potential therapeutic targets of ferroptosis signaling pathways for glioblastoma.Frontiers in pharmacology · 2022Review
- Repurposing of Anticancer Stem Cell Drugs in Brain Tumors.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021Review
- Article
- Glycogen synthase kinase 3β inhibition synergizes with PARP inhibitors through the induction of homologous recombination deficiency in colorectal cancer.Cell death & disease · 2021Article
- Glycogen Synthase Kinase-3 Beta Expression Correlates With Worse Overall Survival in Non-Small Cell Lung Cancer-A Clinicopathological Series.Frontiers in oncology · 2021Article
- Glycogen synthase kinase 3β in tumorigenesis and oncotherapy (Review).Oncology reports · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is the most malignant and lethal subtype brain tumors with high risk of recurrence and therapeutic resistance. Emerging evidence has indicated that glycogen synthesis kinase 3 (GSK3)β plays oncogenic roles in multiple tumor types; however, the underlying mechanisms remain largely unknown. It has also been demonstrated that p53 binding protein 1 (53BP1) plays a central role in DNA double-strand break (DSB) repair. This study aimed to reveal the significance of GSK3β translocation from the cytoplasm to the nucleus, and to determine whether GSK3β induces DNA DSB repair in the nuclei of glioblastoma cells via phospho-53BP1. By performing in vitro experiments, we found that GSK3β translocated from the cytoplasm to the nucleus, and it then bound to 53BP1 following exposure to IR (IR). In addition, 53BP1-mediated DNA DSB repair was observed to be abrogated by the inhibition of GSK3β. Further experiments on the phosphorylation site of 53BP1 by GSK3β revealed that the S/T-Q motif may play a critical role. Importantly, our in vivo and in vitro data clearly indicated that GSK3β induced the phosphorylation of 53BP1 at the Ser166 site. Moreover, brain tumor xenograft models revealed that following exposure to IR plus SB216763, a specific GSK3β inhibitor, tumor growth was markedly inhibited and the survival of mice markedly increased. Based on these results, we concluded that the phosphorylation of 53BP1 by GSK3β was indispensable for DNA DSB repair. Our study also suggested that the inhibition of GSK3β by SB216763 significantly inhibited the proliferation and induced the apoptosis of glioblastoma cells. Taken together, our data indicate that GSK3β, a key phosphorylation protein for 53BP1, may be a potential target for enhancing the sensitivity of glioblastoma cells to radiation.
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