ArticleClinical and translational medicine2022
NAT10: An RNA cytidine transferase regulates fatty acid metabolism in cancer cells.
Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 57 citations in OpenAlex.
- RNA N4-acetylcytidine modification in health and cancer: molecular mechanisms, cellular plasticity, and therapeutic opportunities.Biomarker research · 2026Review
- N-Acetyltransferase 10 (NAT10) at the crossroads of metabolism, immunology, and cancer biology.Cancer metastasis reviews · 2026Review
- Targeting NAT10 with Remodelin reshapes the pro-fibrotic microenvironment in renal fibrogenesisActa pharmaceutica Sinica. B · 2026Article
- The functions, mechanisms and clinical relevance of RNA and protein acetyltransferase NAT10: a comprehensive review.Cell biology and toxicology · 2026Review
- RNA acetylation modification ac4C: An emerging regulatory hub of RNA metabolism disruption in Alzheimer's disease.Molecular biology reports · 2026Review
- Integrative interpretable learning reveals shared patterns of epitranscriptomic regulation across multiple cancer types.BMC biology · 2026Article
- Review
- RNA N4-acetylcytidine modification in human cancers: from molecular function to oncogenic mechanisms.iScience · 2026Review
- The NAT10/acCell communication and signaling : CCS · 2026Review
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- METTL3 safeguard cancer cells from programmed cell death during detachment from their surrounding extracellular matrix.Apoptosis : an international journal on programmed cell death · 2026Article
- Multi-omics characterization of RNA modification enzymes identifies NAT10 as a functionally validated prognostic biomarker in hepatocellular carcinoma.Frontiers in immunology · 2026Article
- NAT10: a potential factor to reverse tumor chemotherapy resistance and radioresistance (Review).Frontiers in immunology · 2026Review
- N4-acetylcytidine modification bridges metabolic reprogramming and immune evasion in cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- RNA modifications in health and disease: from mechanistic insights to therapeutic applications.Precision clinical medicine · 2025Review
- NAT10-mediated lipid metabolic reprogramming drives EGFR-TKI resistance in non-small cell lung cancer via ac4C-dependent mRNA stabilization.Experimental hematology & oncology · 2025Article
- N4-acetylcytidine-mediated SOAT1 upregulation aggravates heart failure by inducing NCOA4-dependent ferroautophagy and ferroptosis in cardiomyocytes.Cellular and molecular life sciences : CMLS · 2025Article
- NAT10 promotes glycolysis and cell stemness of ovarian cancer cells via ac4C acetylation of PGAM1 mRNA.Scientific reports · 2025Article
- NAT10-mediated N4-acetylcytidine modification in KLF9 mRNA promotes adipogenesis.Cell death and differentiation · 2025Article
- NAT10-mediated ac4C modification of Lipin1 mRNA contributes to the pathogenesis of PWMI.JCI insight · 2025Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundN-4 cytidine acetylation (ac4C) is an epitranscriptomics modification catalyzed by N-acetyltransferase 10 (NAT10); important for cellular mRNA stability, rRNA biogenesis, cell proliferation and epithelial to mesenchymal transition (EMT). However, whether other crucial pathways are regulated by NAT10-dependent ac4C modification in cancer cells remains unclear. Therefore, in this study, we explored the impact of NAT10 depletion in cancer cells using unbiased RNA-seq.
methodsHigh-throughput sequencing of knockdown NAT10 in cancer cells was conducted to identify enriched pathways. Acetylated RNA immunoprecipitation-seq (acRIP-seq) and RIP-PCR were used to map and determine ac4C levels of RNA. Exogenous palmitate uptake assay was conducted to assess NAT10 knockdown cancer cells using Oil Red O staining and lipid content analysis. Gas-chromatography-tandem mass spectroscopy (GC/MS) was used to perform untargeted lipidomics.
resultsHigh-throughput sequencing of NAT10 knockdown in cancer cells revealed fatty acid (FA) metabolism as the top enriched pathway through the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis in differentially downregulated genes. FA metabolic genes such as ELOLV6, ACSL1, ACSL3, ACSL4, ACADSB and ACAT1 were shown to be stabilised via NAT10-dependent ac4C RNA acetylation. Additionally, NAT10 depletion was shown to significantly reduce the levels of overall lipid content, triglycerides and total cholesterol. Further, NAT10 depletion in palmitate-loaded cancer cells showed decrease in ac4C levels across the RNA transcripts of FA metabolic genes. In untargeted lipidomics, 496 out of 2 279 lipids were statistically significant in NAT10 depleted cancer cells, of which pathways associated with FA metabolism are the most enriched.
conclusionsConclusively, our results provide novel insights into the impact of NAT10-mediated ac4C modification as a crucial regulatory factor during FA metabolism and showed the benefit of targeting NAT10 for cancer treatment.
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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.