ArticleInternational journal of molecular sciences2023
Sp1 Upregulation Bolsters the Radioresistance of Glioblastoma Cells by Promoting Double Strand Breaks Repair.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed, 4 citations in OpenAlex.
- FLASH Radiotherapy and Organelle-Targeted Radiosensitization in Glioblastoma: A Conceptual and Translational Review.Cancers · 2026Review
- Construction of an actin cytoskeleton-related gene signature for predicting prognosis and therapeutic response in glioblastoma: based on machine learning.Translational cancer research · 2026Article
- Combinatorial functionomics identifies HDAC6-dependent molecular vulnerability of radioresistant head and neck cancer.Experimental hematology & oncology · 2025Article
- Genistein Implications in Radiotherapy: Kill Two Birds with One Stone.Molecules (Basel, Switzerland) · 2025Review
- SP1 undergoes phase separation and activates RGS20 expression through super-enhancers to promote lung adenocarcinoma progression.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Radioresistance remains a critical obstacle in the clinical management of glioblastoma (GBM) by radiotherapy. Therefore, it is necessary to explore the molecular mechanisms underlying radioresistance to improve patient response to radiotherapy and increase the treatment efficacy. The present study aimed to elucidate the role of specificity protein 1 (Sp1) in the radioresistance of GBM cells. Different human GBM cell lines and tumor-bearing mice were exposed to ionizing radiation (IR). Cell survival was determined by the colony formation assay. The expression of genes and proteins in the cells and tissues was analyzed by RT-PCR and western blotting, respectively. The γ-H2AX, p-Sp1 and dependent protein kinase catalytic subunit (DNA-PKcs phospho S2056) foci were analyzed by immunofluorescence. Apoptotic rates were measured by flow cytometry. Sp1 was upregulated after IR in vitro and in vivo and knocking down Sp1-sensitized GBM cells to IR. Sp1 activated the DNA-PKcs promoter and increased its expression and activity. Furthermore, the loss of Sp1 delayed double-strand breaks (DSB) repair and increased IR-induced apoptosis of GBM cells. Taken together, IR upregulates Sp1 expression in GBM cells, enhancing the activity of DNA-PKcs and promoting IR-induced DSB repair, thereby leading to increased radioresistance.
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Registered trials
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