ReviewiScience2026
RNA N4-acetylcytidine modification in human cancers: from molecular function to oncogenic mechanisms.
Review in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- NAT10 promotes colon cancer progression by enhancing predicted N4-acetylcytidine modification of Notch2 mRNA.Discover oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RNA epitranscriptome represents a critical layer of gene regulation, with N4-acetylcytidine (ac4C) emerging as a pivotal modification in cancer biology. Catalyzed exclusively by N-acetyltransferase 10 (NAT10), ac4C decorates a broad spectrum of RNAs, profoundly influencing their stability and translation efficiency. This review synthesizes recent advances illuminating how the NAT10-ac4C axis drives oncogenic processes, including sustained proliferation, metabolic reprogramming, invasion and metastasis, immunosuppression, and therapy resistance by selectively stabilizing mRNAs encoding key oncoproteins. We detail the molecular mechanisms underpinning these roles across diverse malignancies, highlighting context-dependent functions and intricate cross-talk with other signal pathways. Furthermore, we explore the translational promise of this pathway, discussing NAT10 inhibitors and rational combination therapies that resensitize tumors to conventional treatments in preclinical models. Unraveling the full regulatory circuitry of ac4C will not only deepen our understanding of cancer pathogenesis but also pave the way for novel diagnostic and therapeutic strategies in precision oncology.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.