ArticleCancer science2024
NAT10 inhibition promotes ac4C-dependent ferroptosis to counteract sorafenib resistance in nasopharyngeal carcinoma.
Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- LINC00839 transcriptionally activated by ELK1 represses ferroptosis in nasopharyngeal carcinoma by regulating UPF1/RCHY1/DJ-1 axis.NPJ precision oncology · 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
- LINC-AC092535.5 regulates MICAL2 mRNA level to inhibit p53-mediated ferroptosis in nasopharyngeal carcinoma.Oncogene · 2026Article
- RNA modifications and cancer ferroptosis.Cancer cell international · 2026Review
- 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 as a central node in cancer biology: integrating epitranscriptomic regulation, metabolic reprogramming, and immune modulation.Frontiers in immunology · 2026Review
- Targeting NAT10 with Remodelin in cancer drug resistance: mechanisms, preclinical evidence, and combination strategies.Frontiers in pharmacology · 2026Review
- NAT10: a potential factor to reverse tumor chemotherapy resistance and radioresistance (Review).Frontiers in immunology · 2026Review
- Functional roles and mechanisms of NAT10-mediated RNA acFrontiers in cell and developmental biology · 2026Review
- The function of NAT10-driven N4-acetylcytidine modification in cancer: novel insights and potential therapeutic targets.Cell & bioscience · 2025Review
- PTBP1 functions as a suppressor of ferroptosis in endometrial carcinoma cells by stabilizing SLC7A11 mRNA.Discover oncology · 2025Article
- Targeting Ferroptosis in Nasopharyngeal Carcinoma: Mechanisms, Resistance, and Precision Therapeutic Opportunities.International journal of molecular sciences · 2025Review
- Epitranscriptomic modifications in programmed cell death: mechanistic insights and implications for liver diseases.Cellular & molecular biology letters · 2025Review
- Article
- Integrating Single-Cell Transcriptomics and Machine Learning to Define an ac4C Gene Signature in Lung Adenocarcinoma.Thoracic cancer · 2025Article
- Dynamic modifications of circular RNAs drive oncogenesis.Epigenomics · 2025Review
- Emerging role of N-acetyltransferase 10 in diseases: RNA ac4C modification and beyond.Molecular biomedicine · 2025Review
- Solasodine suppresses nasopharyngeal carcinoma progression by inducing ferroptosis.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Sorafenib, an anticancer drug, has been shown to induce ferroptosis in cancer cells. However, resistance to sorafenib greatly limits its therapeutic efficacy, and the exact mechanism of resistance is not fully understood. This study investigated the role of N-Acetyltransferase 10 (NAT10) in influencing the anticancer activity of sorafenib in nasopharyngeal carcinoma (NPC) and its molecular mechanism. NAT10 expression was significantly upregulated in NPC. Mechanistically, NAT10 promotes proteins of solute carrier family 7 member 11 (SLC7A11) expression through ac4C acetylation, inhibiting sorafenib-induced ferroptosis in NPC cells. The combined application of sorafenib and the NAT10 inhibitor remodelin significantly inhibits SLC7A11 expression and promotes ferroptosis in NPC cells. In vivo knockout of NAT10 inhibited the growth of sorafenib-resistant NPC. Our findings suggest that NAT10 inhibition might be a promising therapeutic approach to enhance the anticancer activity of sorafenib.
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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 Socratic graph.