ArticleMolecular neurobiology2022
TRIM56 Reduces Radiosensitization of Human Glioblastoma by Regulating FOXM1-Mediated DNA Repair.
Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- The Regulatory Network of FOXM1: Orchestrating Cancer Progression and Resistance to Therapy.International journal of molecular sciences · 2026Review
- The E3 ubiquitin ligase TRIM56 promotes aggregation and activation of Src protein through Lys63-linked polyubiquitination in hepatocellular carcinoma.Cell death & disease · 2025Article
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- The oncogenic role of TRIM56 in pancreatic cancer via the TRAF6/NF-kB axis.Journal of molecular histology · 2025Article
- DNA-RNA hybrids in inflammation: sources, immune response, and therapeutic implications.Journal of molecular medicine (Berlin, Germany) · 2025Review
- TRIM35 Negatively Regulates the cGAS-STING-Mediated Signaling Pathway by Attenuating K63-Linked Ubiquitination of STING.Inflammation · 2025Article
- The regulation of innate antiviral immunity by TRIM56.Infectious diseases & immunity · 2025Review
- Review
- Forkhead box transcription factors (FOXOs and FOXM1) in glioma: from molecular mechanisms to therapeutics.Cancer cell international · 2023Review
- The Functions of TRIM56 in Antiviral Innate Immunity and Tumorigenesis.International journal of molecular sciences · 2023Review
- TRIM56 acts through the IQGAP1-CDC42 signaling axis to promote glioma cell migration and invasion.Cell death & disease · 2023Article
- TRIM56 promotes malignant progression of glioblastoma by stabilizing cIAP1 protein.Journal of experimental & clinical cancer research : CR · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recurrent glioblastoma is characterized by resistance to radiotherapy or chemotherapy. In this study, we investigated the role of TRIM56 in radiosensitization and its potential underlying molecular mechanism. TRIM56 expression levels were measured in glioblastoma tissues and cell lines by immunohistochemical staining, western blot, and qRT-PCR. MTT assay, colony formation assay, and TUNEL assay were used to investigate the effect of TRIM56 on cell viability, cell proliferation, and cell apoptosis. Co-immunoprecipitation was used to clarify the interaction between TRIM56 and FOXM1. Finally, tumor xenograft experiments were performed to analyze the effect of TRIM56 on tumor growth in vivo. The expression of TRIM56 was significantly increased in glioblastoma tissues and cell lines and its expression was associated with poor prognosis of patients with glioblastoma. Moreover, TRIM56 reduced the radiosensitivity of glioblastoma cells and promoted DNA repairment. Mechanistically, TRIM56 promoted FOXM1 protein level, enhanced the stability of FOXM1 by de-ubiquitination, and promoted DNA damage repair through FOXM1 in glioblastoma cells. TRIM56 could reduce the radiosensitivity of glioblastoma in vivo. TRIM56 may suppress the radiosensitization of human glioblastoma by regulating FOXM1-mediated DNA repair. Targeting the TRIM56 may be an effective method to reverse radiotherapy-resistant in glioblastoma recurrent.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.