ArticleMolecular neurobiology2023
Loss of p53 Concurrent with RAS and TERT Activation Induces Glioma Formation.
Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- p53 in Canine Mammary Tumors: From Molecular Pathogenesis to Biomarker Applications and Comparative Oncology.Veterinary sciences · 2026Review
- Overexpression of EZH2 is associated with clinicopathological parameters and poor prognosis in gliomas.Oncology letters · 2026Article
- EZH2 inhibition and 5-azacytidine enhance antitumor immunity in PTEN-deficient glioblastoma by activation viral mimicry response.Journal for immunotherapy of cancer · 2025Article
- Telomeres, telomerase, and cancer: mechanisms, biomarkers, and therapeutics.Experimental hematology & oncology · 2025Review
- Advances of Protein Palmitoylation in Tumor Cell Deaths.Cancers · 2023Review
- The role of s-palmitoylation in neurological diseases: implication for zDHHC family.Frontiers in pharmacology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
There is an ongoing debate regarding whether gliomas originate due to functional or genetic changes in neural stem cells (NSCs). Genetic engineering has made it possible to use NSCs to establish glioma models with the pathological features of human tumors. Here, we found that RAS, TERT, and p53 mutations or abnormal expression were associated with the occurrence of glioma in the mouse tumor transplantation model. Moreover, EZH2 palmitoylation mediated by ZDHHC5 played a significant role in this malignant transformation. EZH2 palmitoylation activates H3K27me3, which in turn decreases miR-1275, increases glial fibrillary acidic protein (GFAP) expression, and weakens the binding of DNA methyltransferase 3A (DNMT3A) to the OCT4 promoter region. Thus, these findings are significant because RAS, TERT, and p53 oncogenes in human neural stem cells are conducive to a fully malignant and rapid transformation, suggesting that gene changes and specific combinations of susceptible cell types are important factors in determining the occurrence of gliomas.
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Registered trials
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