ArticleOncogene2023
N4-acetylcytidine modification of lncRNA CTC-490G23.2 promotes cancer metastasis through interacting with PTBP1 to increase CD44 alternative splicing.
Article in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 75 citations in OpenAlex.
- RNA N4-acetylcytidine modification in health and cancer: molecular mechanisms, cellular plasticity, and therapeutic opportunities.Biomarker research · 2026Review
- LncRNA-driven alternative splicing landscapes associate with survival outcomes in ovarian cancer.Non-coding RNA research · 2026Article
- Review
- The functions, mechanisms and clinical relevance of RNA and protein acetyltransferase NAT10: a comprehensive review.Cell biology and toxicology · 2026Review
- NAT10 inhibition alleviates renal tubular epithelial cell senescence by impeding ac4C acetylation of PAPP-A mRNA in diabetic nephropathy.Cell death & disease · 2026Article
- Insights into the therapeutic strategies for aging and aging-associated diseases.Signal transduction and targeted therapy · 2026Review
- Integrative interpretable learning reveals shared patterns of epitranscriptomic regulation across multiple cancer types.BMC biology · 2026Article
- Review
- N4-acetylcytidine in LncRNA Gm26917 Promotes Translation in Female Germline Stem Cells by Recruiting Ribosomal Protein mRNA via EEF1A1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- RNA N4-acetylcytidine modification in human cancers: from molecular function to oncogenic mechanisms.iScience · 2026Review
- The NAT10/acCell communication and signaling : CCS · 2026Review
- NAT10 and ac4C modification in cancer immunity and metabolism: emerging mechanisms and therapeutic potential.Journal of translational medicine · 2026Review
- NAT10 Promotes Tubular Epithelial Cell Senescence in Cisplatin-Induced Acute Kidney Injury by Regulating DDX17.International journal of biological sciences · 2026Article
- Functional roles and mechanisms of NAT10-mediated RNA acFrontiers in cell and developmental biology · 2026Review
- N4-acetylcytidine modification bridges metabolic reprogramming and immune evasion in cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- The cancer-testis lncRNA LINC01940 promotes gastric cancer malignant progression and chemoresistance by enhancing ribosome biogenesis via TAF15-mediated NOL11 SUMOylation.Cellular & molecular biology letters · 2025Article
- Advances in RNA modification in myocardial fibrosis (Review).International journal of molecular medicine · 2025Review
- NAT10-mediated ac4C modification of KDM1B drives osteoarthritis progression through epigenetic suppression of SOX9.Cellular and molecular life sciences : CMLS · 2025Article
- NAT10 induces N4-acetylcytidine modification of AdipoR1-mediated mitochondrial biogenesis against endothelial-to-mesenchymal transition in hypertension.Molecular medicine (Cambridge, Mass.) · 2025Article
- NAT10 Increases Lysosomal Acidification to Promote Esophageal Cancer Metastasis via ac4C Acetylation of ATP6V0E1 mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although N4-acetylcytidine (ac4C) modification affects the stability and translation of mRNA, it is unknown whether it exists in noncoding RNAs, and its biological function is unclear. Here, nucleotide-resolution method for profiling CTC-490G23.2 ac4C sites and gain- and loss-of-function experiments revealed that N-acetyltransferase 10 (NAT10) is responsible for ac4C modification of long noncoding RNAs (lncRNAs). NAT10-mediated ac4C modification leads to the stabilization and overexpression of lncRNA CTC-490G23.2 in primary esophageal squamous cell carcinoma (ESCC) and its further upregulation in metastatic tissues. CTC-490G23.2 significantly promotes cancer invasion and metastasis in vitro and in vivo. Mechanistically, CTC-490G23.2 acts as a scaffold to increase the binding of CD44 pre-mRNA to polypyrimidine tract-binding protein 1 (PTBP1), resulting in a oncogenic splicing switch from the standard isoform CD44s to the variant isoform CD44v(8-10). CD44v(8-10), but not CD44s, binds to and increases the protein stability of vimentin. Expression levels of CTC-490G23.2 and CD44v(8-10) can predict poor prognosis in cancer patients. Furthermore, the antisense oligonucleotide (ASO)/SV40-LAH4-L1 peptide self-assembled nanocomplexes targeting CTC490G23.2 exerts a significantly suppressive effect on cancer metastasis. The outcome of this study will provide new mechanistic insight into the ac4C modification of lncRNAs and useful clues for the development of novel systemic therapies and prognostic biomarkers.
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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.