ArticleFrontiers in immunology2023
Immune response and drug therapy based on ac4C-modified gene in pancreatic cancer typing.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 21 citations in OpenAlex.
- RNA N4-acetylcytidine modification in health and cancer: molecular mechanisms, cellular plasticity, and therapeutic opportunities.Biomarker research · 2026Review
- An ac4C-CDK4 regulatory axis driven by NAT10 sustains proliferative signaling in colorectal cancer.Translational oncology · 2026Article
- Integrative interpretable learning reveals shared patterns of epitranscriptomic regulation across multiple cancer types.BMC biology · 2026Article
- Review
- NAT10 promotes cisplatin resistance and immune escape by increasing the expression of DUSP1 and PD-L1 in gastric cancer.Cell death discovery · 2026Article
- Integrative profiling of diverse post-translational modifications for prognostic stratification and personalized therapy in papillary thyroid cancer.Frontiers in endocrinology · 2026Article
- NAT10: a potential factor to reverse tumor chemotherapy resistance and radioresistance (Review).Frontiers in immunology · 2026Review
- The function of NAT10-driven N4-acetylcytidine modification in cancer: novel insights and potential therapeutic targets.Cell & bioscience · 2025Review
- Targeted NAT10 Degradation by PROTAC NP1192 Suppresses Hypoxia-Adaptive Glycolysis and Reinvigorates CD8ACS central science · 2025Article
- Targeting the ac4C 'Writer' NAT10 enhances pancreatic cancer immunotherapy via dual modulation of CD8+ T cells and tumor cells.Cell death & disease · 2025Article
- Roles of RNA modifications in aging and age-related diseases.BMB reports · 2025Review
- Article
- Biological function and mechanism of NAT10 in cancer.Cancer innovation · 2025Review
- Research progress on NAT10-mediated acetylation in normal development and disease.Frontiers in cell and developmental biology · 2025Review
- Acetyltransferase NAT10 promotes an immunosuppressive microenvironment by modulating CD8Molecular biomedicine · 2024Article
- The role and mechanism of NAT10-mediated ac4C modification in tumor development and progression.MedComm · 2024Review
- PCBP1/2 and TDP43 Function as NAT10 Adaptors to Mediate mRNA acAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Remodelin delays non-small cell lung cancer progression by inhibiting NAT10 via the EMT pathway.Cancer medicine · 2024Article
- Dissecting the oncogenic properties of essential RNA-modifying enzymes: a focus on NAT10.Oncogene · 2024Review
- CircMAST1 inhibits cervical cancer progression by hindering the N4-acetylcytidine modification of YAP mRNA.Cellular & molecular biology letters · 2024Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-4 cytidine acetylation (ac4C) is an epitranscriptome modification catalyzed by N-acetyltransferase 10 (NAT10) and is essential for cellular mRNA stability, rRNA biosynthesis, cell proliferation, and epithelial-mesenchymal transition (EMT). Numerous studies have confirmed the inextricable link between NAT10 and the clinical characteristics of malignancies. It is unclear, however, how NAT10 might affect pancreatic ductal adenocarcinoma. We downloaded pancreatic ductal adenocarcinoma patients from the TCGA database. We obtained the corresponding clinical data for data analysis, model construction, differential gene expression analysis, and the GEO database for external validation. We screened the published papers for NAT10-mediated ac4C modifications in 2156 genes. We confirmed that the expression levels and genomic mutation rates of NAT10 differed significantly between cancer and normal tissues. Additionally, we constructed a NAT10 prognostic model and examined immune infiltration and altered biological pathways across the models. The NAT10 isoforms identified in this study can effectively predict clinical outcomes in pancreatic ductal adenocarcinoma. Furthermore, our study showed that elevated levels of NAT10 expression correlated with gemcitabine resistance, that aberrant NAT10 expression may promote the angiogenic capacity of pancreatic ductal adenocarcinoma through activation of the TGF-β pathway, which in turn promotes distal metastasis of pancreatic ductal adenocarcinoma, and that NAT10 knockdown significantly inhibited the migration and clonogenic capacity of pancreatic ductal adenocarcinoma cells. In conclusion, we proposed a predictive model based on NAT10 expression levels, a non-invasive predictive approach for genomic profiling, which showed satisfactory and effective performance in predicting patients' survival outcomes and treatment response. Medicine and electronics will be combined in more interdisciplinary areas in the future.
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