ArticleThoracic cancer2024
NAT10-mediated mRNA N4-acetylcytidine modification of MDR1 and BCRP promotes breast cancer progression.
Article in Thoracic cancer, 2024. 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, 16 citations in OpenAlex.
- 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
- Integrative interpretable learning reveals shared patterns of epitranscriptomic regulation across multiple cancer types.BMC biology · 2026Article
- Review
- NAT10: a potential factor to reverse tumor chemotherapy resistance and radioresistance (Review).Frontiers in immunology · 2026Review
- N4-acetylcytidine modification bridges metabolic reprogramming and immune evasion in cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- 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
- Functional roles and mechanisms of NAT10-mediated RNA acFrontiers in cell and developmental biology · 2026Review
- NAT10 as a central node in cancer biology: integrating epitranscriptomic regulation, metabolic reprogramming, and immune modulation.Frontiers in immunology · 2026Review
- NAT10-mediated N4-acetylcytidine (ac4C) modification of PIK3R2 mRNA promotes malignant progression of glioblastoma.Cell death & disease · 2025Article
- Targeting NAT10 Inhibits Hepatocarcinogenesis via ac4C-Mediated SMAD3 mRNA Stability.Exploration (Beijing, China) · 2025Article
- The function of NAT10-driven N4-acetylcytidine modification in cancer: novel insights and potential therapeutic targets.Cell & bioscience · 2025Review
- NAT10 promotes glycolysis and cell stemness of ovarian cancer cells via ac4C acetylation of PGAM1 mRNA.Scientific reports · 2025Article
- Article
- Emerging roles of RNA N4-acetylcytidine modification in reproductive health.Protein & cell · 2025Review
- NAT10 inhibits the pyroptosis of laryngeal squamous cell carcinoma through ac4C modification of ELANE mRNA.BMC cancer · 2025Article
- NAT10 mediates TLR2 to promote podocyte senescence in adriamycin-induced nephropathy.Cell death & disease · 2025Article
- The N-acetyltransferase 10 inhibitor [EJNMMI radiopharmacy and chemistry · 2025Article
- Molecular mechanisms and therapeutic strategies in overcoming chemotherapy resistance in cancer.Molecular biomedicine · 2025Review
- Review
- The role and mechanism of NAT10-mediated ac4C modification in tumor development and progression.MedComm · 2024Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundN-acetyltransferase 10 (NAT10) serves as a critical enzyme in mediating the N4-acetylcytidine (ac4C) that ensures RNA stability and effective translation processes. The role of NAT10 in driving the advancement of breast cancer remains uninvestigated.
methodsWe observed an increase in NAT10 expression, both at mRNA level through the analysis of the Cancer Genome Atlas (TCGA) database and at the protein level of tumor tissues from breast cancer patients. We determined that a heightened expression of NAT10 served as a predictor of an unfavorable clinical outcome. By screening the Cancer Cell Line Encyclopedia (CCLE) cell bank, this expression pattern of NAT10 was consistency found across almost all the classic breast cancer cell lines.
resultsFunctionally, interference of NAT10 expression exerts an inhibitory effect on proliferation and invasion of breast cancer cells. By using ac4C RNA immunoprecipitation (ac4c-RIP) and acRIP-qPCR assays, we identified a reduction of ac4C enrichment within the ATP binding cassette (ABC) transporters, multidrug resistance protein 1 (MDR1) and breast cancer resistance protein (BCRP), consequent to NAT10 suppression. Expressions of MDR1 and BCRP exhibited a positive correlation with NAT10 expression in tumor tissues, and the inhibition of NAT10 in breast cancer cells resulted in a decrease of MDR1 and BCRP expression. Therefore, the overexpressing of MDR1 and BCRP could partially rescue the adverse consequences of NAT10 depletion. In addition, we found that, remodelin, a NAT10 inhibitor, reinstated the susceptibility of capecitabine-resistant breast cancer cells to the chemotherapy, both in vitro and in vivo.
conclusionThe results of our study demonstrated the essential role of NAT10-mediated ac4c-modification in breast cancer progression and provide a novel strategy for overcoming chemoresistance challenges.
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