ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023
NAT10/ac4C/FOXP1 Promotes Malignant Progression and Facilitates Immunosuppression by Reprogramming Glycolytic Metabolism in Cervical Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.
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Who cites it
113 citing papers in PubMed, 97 citations in OpenAlex.
- Overexpression of SLC44A4 suppresses ferroptosis and reduces lipid peroxidationAnnals of medicine · 2026Article
- RNA N4-acetylcytidine modification in health and cancer: molecular mechanisms, cellular plasticity, and therapeutic opportunities.Biomarker research · 2026Review
- Article
- NAT10 aggravates psoriasis by promoting keratinocytes fatty acid synthesis via stable FASN transcription.Journal of pharmaceutical analysis · 2026Article
- NAT10 promotes prostate cancer progression by acetylating mRNA of MARK2 and activating mTOR/HIF-1α/C-Myc pathway to enhance glycolytic reprogramming.Cancer gene therapy · 2026Article
- N-Acetyltransferase 10 (NAT10) at the crossroads of metabolism, immunology, and cancer biology.Cancer metastasis reviews · 2026Review
- RNA modifications in cancer: regulators of tumor evolution and therapeutic response.Molecular cancer · 2026Review
- The functions, mechanisms and clinical relevance of RNA and protein acetyltransferase NAT10: a comprehensive review.Cell biology and toxicology · 2026Review
- Cuproptosis and Mitophagy Mediated by the THUMPD1/IGF2R-Dependent Suppression of AKT and Activation of AMPK Signaling Suppress Lung Adenocarcinoma Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The NAT10/c-Myc positive feedback loop orchestrates tRNA acCellular & molecular biology letters · 2026Article
- Targeted delivery of TGF-β inhibitor via LHRH-NanoTi reverses the NAT10/ac4C-mediated cisplatin-induced immunosuppressive tumor microenvironment in ovarian cancer.Journal of nanobiotechnology · 2026Article
- The role of tumor metabolic reprogramming in acquired anti-PD-1/PD-L1 resistance.Translational lung cancer research · 2026Review
- Lactate and lactylation: mechanisms, function, diseases, and therapeutic targets.Molecular biomedicine · 2026Review
- NAT10/acProceedings of the National Academy of Sciences of the United States of America · 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
- NAT10 drives ovarian cancer progression via NLRP3 mRNA ac4C modification.Discover oncology · 2026Article
- RILPL2 suppresses metabolic reprogramming and progression of cervical cancer by attenuating LDHA protein stability and inhibiting H3K18 lactylation.Cell death & disease · 2026Article
- Review
- RNF112 mediates immunosuppression to inhibit the proliferation of cervical cancer by Foxm1.Translational cancer research · 2026Article
53 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 7 institutions in 2 countries.
Funding
Abstract
Immunotherapy has recently emerged as the predominant therapeutic approach for cervical cancer (CCa), driven by the groundbreaking clinical achievements of immune checkpoint inhibitors (ICIs), such as anti-PD-1/PD-L1 antibodies. N4-acetylcytidine (ac4C) modification, catalyzed by NAT10, is an important posttranscriptional modification of mRNA in cancers. However, its impact on immunological dysregulation and the tumor immunotherapy response in CCa remains enigmatic. Here, a significant increase in NAT10 expression in CCa tissues is initially observed that is clinically associated with poor prognosis. Subsequently, it is found that HOXC8 activated NAT10 by binding to its promoter, thereby stimulating ac4C modification of FOXP1 mRNA and enhancing its translation efficiency, eventually leading to induction of GLUT4 and KHK expression. Moreover, NAT10/ac4C/FOXP1 axis activity resulted in increased glycolysis and a continuous increase in lactic acid secretion by CCa cells. The lactic acid-enriched tumor microenvironment (TME) further contributed to amplifying the immunosuppressive properties of tumor-infiltrating regulatory T cells (Tregs). Impressively, NAT10 knockdown enhanced the efficacy of PD-L1 blockade-mediated tumor regression in vivo. Taken together, the findings revealed the oncogenic role of NAT10 in initiating crosstalk between cancer cell glycolysis and immunosuppression, which can be a target for synergistic PD-1/PD-L1 blockade immunotherapy in CCa.
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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.