ReviewCell & bioscience2025
The function of NAT10-driven N4-acetylcytidine modification in cancer: novel insights and potential therapeutic targets.
Review in Cell & bioscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- An ac4C-CDK4 regulatory axis driven by NAT10 sustains proliferative signaling in colorectal cancer.Translational oncology · 2026Article
- NAT10-mediated N4-acetylcytidine modification drives RNA splicing of PML to alleviate adipose-derived stem cell senescence and promote diabetic wound healing.Clinical and translational medicine · 2026Article
- ac4C modification sites prediction in human mRNA: a complete review.Briefings in bioinformatics · 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
N4-acetylcytidine (ac4C) is a novel RNA modification that plays important biological roles in a variety of diseases, including tumors, by regulating gene expression at the posttranscriptional level. As a currently known ac4C-modified "writing" protein, N-acetyltransferase (NAT10) affects the stability and translation efficiency of target mRNAs by changing the chemical and spatial structure of RNA, thereby acting as an oncogene and tumor suppressor gene in different tumors, highlighting its potential role as a tumor prognostic marker and therapeutic target. Research on the molecular mechanism of ac4C modification and its function in tumors continues to expand, but its action network and clinical translational application still face many challenges. This review systematically explains the molecular mechanism of ac4C modification and its biological significance in tumors and its connection with relevant signaling pathways and the immune microenvironment, focuses on analyzing the research progress of ac4C modification enzymes, and discusses its potential as a tumor target. The purpose of this study was to provide a theoretical basis and new ideas for basic research and the clinical translation of the ac4C modification in the field of oncology.
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What Socratic holds
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.