ArticleCell death & disease2023
N4-acetylcytidine-dependent GLMP mRNA stabilization by NAT10 promotes head and neck squamous cell carcinoma metastasis and remodels tumor microenvironment through MAPK/ERK signaling pathway.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 42 citations in OpenAlex.
- Targeting NAT10 Activates Tumor-Intrinsic Immunity and Suppresses Tumor Progression in Head and Neck Squamous Cell Carcinoma.bioRxiv : the preprint server for biology · 2026Article
- YBX1 Promotes Malignant Progression of HNSCC via Stabilizing NSUN2-m5C Modified ATF4 mRNA.Cancer science · 2026Article
- NAT10 promotes colon cancer progression by enhancing predicted N4-acetylcytidine modification of Notch2 mRNA.Discover oncology · 2026Article
- Programmable RNA acetylation with CRISPR-Cas13.Nature chemical biology · 2026Article
- Integrative interpretable learning reveals shared patterns of epitranscriptomic regulation across multiple cancer types.BMC biology · 2026Article
- Epitranscriptomic control of cancer: the emerging roles of m⁵C and ac⁴C RNA modifications.Cell death discovery · 2026Review
- Microglial cholesterol reprogramming drives cognitive impairment under hypobaric hypoxia.Journal of neuroinflammation · 2026Article
- A comprehensive analysis of the use of nucleoside analogues in RNA therapeutics.Journal of translational medicine · 2026Review
- Quetiapine inhibits the oxidative phosphorylation in head and neck squamous cell carcinoma through suppressing NAT10-mediated ac4C modification.Translational cancer research · 2026Article
- Dynamic regulation of mRNA acetylation at synapses by spatial memory in mouse hippocampus.eLife · 2026Article
- NAT10-mediated ac4C RNA acetylation stabilizes CXCL5/DEK mRNA to drive proliferation and metastasis in lung adenocarcinoma.Cell death & disease · 2026Article
- RNA N4-acetylcytidine modification in human cancers: from molecular function to oncogenic mechanisms.iScience · 2026Review
- NAT10 and ac4C modification in cancer immunity and metabolism: emerging mechanisms and therapeutic potential.Journal of translational medicine · 2026Review
- NAT10 drives hepatocellular carcinoma progression through SQLE-mediated cholesterol biosynthesis and is targetable by remodelin.iScience · 2026Article
- Development and Validation of an UPLC-MS/MS Method for Remodelin Quantification in Mouse Plasma and Tissues: Application to Biodistribution and Ultrastructural Assessment.Journal of analytical methods in chemistry · 2026Article
- N4-acetylcytidine modification bridges metabolic reprogramming and immune evasion in cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- NAT10 as a central node in cancer biology: integrating epitranscriptomic regulation, metabolic reprogramming, and immune modulation.Frontiers in immunology · 2026Review
- RNA modifications in health and disease: from mechanistic insights to therapeutic applications.Precision clinical medicine · 2025Review
- Trained Immunity Exacerbates Inflammatory Arthritis Progression via Promoting Synovial Fibroblast Ferroptotic Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The function of NAT10-driven N4-acetylcytidine modification in cancer: novel insights and potential therapeutic targets.Cell & bioscience · 2025Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N4-acetylcytidine (ac4C) is a post-transcriptional RNA modification that regulates in various important biological processes. However, its role in human cancer, especially lymph node metastasis, remains largely unknown. Here, we demonstrated N-Acetyltransferase 10 (NAT10), as the only known "writer" of ac4C mRNA modification, was highly expressed in head and neck squamous cell carcinoma (HNSCC) patients with lymph node metastasis. High NAT10 levels in the lymph nodes of patients with HNSCC patients are a predictor of poor overall survival. Moreover, we found that high expression of NAT10 was positively upregulated by Nuclear Respiratory Factor 1 (NRF1) transcription factor. Gain- and loss-of-function experiments displayed that NAT10 promoted cell metastasis in mice. Mechanistically, NAT10 induced ac4C modification of Glycosylated Lysosomal Membrane Protein (GLMP) and stabilized its mRNA, which triggered the activation of the MAPK/ERK signaling pathway. Finally, the NAT10-specific inhibitor, remodelin, could inhibit HNSCC tumorigenesis in a 4-Nitroquinoline 1-oxide (4NQO)-induced murine tumor model and remodel the tumor microenvironment, including angiogenesis, CD8
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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.