ArticleCell death & disease2025
NAT10-mediated N4-acetylcytidine (ac4C) modification of PIK3R2 mRNA promotes malignant progression of glioblastoma.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- An ac4C-CDK4 regulatory axis driven by NAT10 sustains proliferative signaling in colorectal cancer.Translational oncology · 2026Article
- Functional roles and mechanisms of NAT10-mediated RNA acFrontiers in cell and developmental biology · 2026Review
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Authors and funding
13 authors.
Funding
Abstract
Glioma is the most common primary tumor in the central nervous system, with glioblastoma (GBM) representing one of the most malignant forms, accounting for 46.1% of cases. GBM is characterized by rapid progression, high malignancy, and poor prognosis, with median survival remaining less than 15 months despite combined surgery, radiotherapy, and chemotherapy. NAT10, the only known acetyltransferase mediating N4-acetylcytidine (ac4C) modification in eukaryotes, has been implicated in promoting tumorigenesis and progression in colon cancer, bladder cancer, pancreatic ductal cancer, among others. In this study, we found that NAT10 is highly expressed in GBM and is positively correlated with malignant pathological features and poor prognosis in patients. In vitro experiments demonstrated that NAT10 promotes tumor proliferation, migration, and invasion. In vivo experiments further confirmed that NAT10 facilitates malignant progression of tumors. Mechanistically, we revealed that NAT10 regulates PIK3R2 stabilization through ac4C modification, thereby participating malignant characterization of GBM. Additionally, our data demonstrated a positive correlation between NAT10 and PIK3R2 in glioma patients. Taken together, our findings strongly suggest that NAT10 is a potential therapeutic target for GBM.
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