ReviewMedComm2024
The role and mechanism of NAT10-mediated ac4C modification in tumor development and progression.
Review in MedComm, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed.
- An ac4C-CDK4 regulatory axis driven by NAT10 sustains proliferative signaling in colorectal cancer.Translational oncology · 2026Article
- Cuproptosis and Mitophagy Mediated by the THUMPD1/IGF2R-Dependent Suppression of AKT and Activation of AMPK Signaling Suppress Lung Adenocarcinoma Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Integrative interpretable learning reveals shared patterns of epitranscriptomic regulation across multiple cancer types.BMC biology · 2026Article
- NAT10/acProceedings of the National Academy of Sciences of the United States of America · 2026Article
- The Role of NAT10-Mediated ac4C Modification in Osteoblast Function and Bone Formation: Insights from Integrative Bioinformatics and Experimental Validation.Physiological research · 2026Article
- ac4C modification sites prediction in human mRNA: a complete review.Briefings in bioinformatics · 2026Review
- Review
- NAT10 promotes gallbladder cancer progression by remodeling cholesterol metabolism via PCSK9 mRNA acetylation.Cell death discovery · 2026Article
- Quetiapine inhibits the oxidative phosphorylation in head and neck squamous cell carcinoma through suppressing NAT10-mediated ac4C modification.Translational cancer research · 2026Article
- Integrated epigenetic networks in aging: from histone to RNA modifications.Journal of translational medicine · 2026Review
- NAT10 and ac4C modification in cancer immunity and metabolism: emerging mechanisms and therapeutic potential.Journal of translational medicine · 2026Review
- HSF4 alleviates ferroptosis in colorectal cancer through transcriptional regulation of MBOAT1/2.Functional & integrative genomics · 2026Article
- WDR5-H3K4me3 Epigenetic Axis Promotes TRMT6-Dependent tRNA MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Regulation of apoptosis, ferroptosis, and pyroptosis mediated by acetylation.Cell death discovery · 2026Review
- NAT10-mediated ac4C modifications regulate glioblastoma progression.Cell death & disease · 2026Article
- Targeting the NAT10-HDAC4 positive feedback loop counteracts immunosuppression in breast cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- NAT10 as a central node in cancer biology: integrating epitranscriptomic regulation, metabolic reprogramming, and immune modulation.Frontiers in immunology · 2026Review
- Targeting NAT10 with Remodelin in cancer drug resistance: mechanisms, preclinical evidence, and combination strategies.Frontiers in pharmacology · 2026Review
- NAT10: a potential factor to reverse tumor chemotherapy resistance and radioresistance (Review).Frontiers in immunology · 2026Review
- RNA epitranscriptomic regulation of tumor immune evasion: mechanisms, context-dependent roles, and therapeutic implications.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RNA modification has emerged as a crucial area of research in epigenetics, significantly influencing tumor biology by regulating RNA metabolism. N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) modification, the sole known acetylation in eukaryotic RNA, influences cancer pathogenesis and progression. NAT10 is the only writer of ac4C and catalyzes acetyl transfer on targeted RNA, and ac4C helps to improve the stability and translational efficiency of ac4C-modified RNA. NAT10 is highly expressed and associated with poor prognosis in pan-cancers. Based on its molecular mechanism and biological functions, ac4C is a central factor in tumorigenesis, tumor progression, drug resistance, and tumor immune escape. Despite the increasing focus on ac4C, the specific regulatory mechanisms of ac4C in cancer remain elusive. The present review thoroughly analyzes the current knowledge on NAT10-mediated ac4C modification in cancer, highlighting its broad regulatory influence on targeted gene expression and tumor biology. This review also summarizes the limitations and perspectives of current research on NAT10 and ac4C in cancer, to identify new therapeutic targets and advance cancer treatment strategies.
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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 Socratic graph.