ArticleClinics (Sao Paulo, Brazil)2025
NAT10-mediated N4-acetylcytosine modification promotes the progression of retinoblastoma by improving the HK1 mRNA stability to enhance glycolysis.
Article in Clinics (Sao Paulo, Brazil), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The trial behind it
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Who cites it
4 citing papers in PubMed.
- RNA N4-acetylcytidine modification in human cancers: from molecular function to oncogenic mechanisms.iScience · 2026Review
- NAT10 promotes the glycolysis of retinoblastoma through ac4C modification of PFKFB3 mRNA.BMC cancer · 2026Article
- NAT10 as a central node in cancer biology: integrating epitranscriptomic regulation, metabolic reprogramming, and immune modulation.Frontiers in immunology · 2026Review
- N4-acetylcytidine modification bridges metabolic reprogramming and immune evasion in cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveRetinoblastoma (RB) is a type of intraocular tumor in childhood with a high lethality rate. N4-acetylcytosine (ac
methodPhenotypically, dot blot assay and quantitative real-time PCR were used to detect the ac
resultsThe present results demonstrated that the levels of ac
conclusionThe authors illustrated that NAT10 plays an important role in the progression of RB by regulating the ac
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Registered trials
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