ReviewCell death discovery2026
Epitranscriptomic control of cancer: the emerging roles of m⁵C and ac⁴C RNA modifications.
Review in Cell death discovery, 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.
- Targeting NAT10 with Remodelin in cancer drug resistance: mechanisms, preclinical evidence, and combination strategies.Frontiers in pharmacology · 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
3 authors.
Funding
Abstract
Cytidine RNA modifications have emerged as key regulators of tumor cancer biology, linking transcriptional control to metabolic adaptation and immune evasion. Among them, 5-methylcytidine (m⁵C) and N⁴-acetylcytidine (ac⁴C) represent dynamic and functionally complementary epitranscriptomic marks that operate through distinct regulatory layers. m⁵C, catalyzed by the NSUN family methyltransferases, primarily stabilizes pro-tumorigenic transcripts, enhances glycolysis, and suppresses antitumor immunity through modulation of cytokine and checkpoint pathways. In parallel, ac⁴C, mediated by the acetyltransferase NAT10, fine-tunes translational efficiency and proteostasis, enabling tumor cells to adapt to metabolic and therapeutic stress. Together, these modifications cooperatively remodel the tumor immune microenvironment by driving macrophage polarization, T-cell exhaustion, and attenuation of interferon signaling, establishing a durable immunosuppressive niche. Notably, pharmacologic or genetic inhibition of m⁵C- and ac⁴C-modifying enzymes reverses malignant phenotypes and restores sensitivity to immune checkpoint and metabolic therapies. Elucidating this two-layer cytidine epitranscriptomic architecture unveils new epigenetic dimensions of tumor plasticity and offers promising avenues for precision RNA-targeted oncology.
Identifiers
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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 OpenQuestion graph.