ArticleScientific reports2025
NAT10 promotes hepatocellular carcinoma progression by modulating the ac4C-DDIAS-PI3K-Akt axis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
The trial behind it
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.
- DUSP12 Regulates NAT10-Mediated RNA Acetylation to Modulate DNA Repair and Therapeutic Response in Hepatocellular Carcinoma.MedComm · 2026Article
- NAT10 promotes the activation of hepatic stellate cells by modulating the TGF-β1-ac4C-COL1A1 axis.Hepatology international · 2026Article
- Quetiapine inhibits the oxidative phosphorylation in head and neck squamous cell carcinoma through suppressing NAT10-mediated ac4C modification.Translational cancer research · 2026Article
- RNA N4-acetylcytidine modification in human cancers: from molecular function to oncogenic mechanisms.iScience · 2026Review
- The NAT10/acCell communication and signaling : CCS · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Primary liver cancer (PLC) is a prevalent tumor globally, ranking third in cancer-related mortality. The role of N4-acetylcysteine (ac4C) and N-acetyltransferase 10 (NAT10) in hepatocellular carcinoma (HCC) progression, migration, and invasion requires further elucidation. High NAT10 expression correlated with poor prognosis in HCC patients. Knockdown of NAT10 hindered HCC cell proliferation. AcRIP-seq screening revealed DDIAS as a significant downstream target of NAT10. Decreased NAT10 levels reduced DDIAS mRNA stability, leading to decreased proliferation, migration, and invasion of HCC cells upon DDIAS knockdown. Ectopic expression of DDIAS counteracted the effects of NAT10 knockdown by modulating the PI3K/AKT pathway. NAT10 was found to be elevated in HCC tissues compared to normal tissues, promoting HCC progression and correlating with shorter overall survival in patients. Mechanistically, NAT10 regulated HCC progression through the ac4C-DDIAS-PI3K-AKT axis.
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Registered trials
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