ArticleCancer medicine2024
Remodelin delays non-small cell lung cancer progression by inhibiting NAT10 via the EMT pathway.
Article in Cancer medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- RNA N4-acetylcytidine modification in health and cancer: molecular mechanisms, cellular plasticity, and therapeutic opportunities.Biomarker research · 2026Review
- NAT10-mediated acJournal of molecular histology · 2026Article
- An ac4C-CDK4 regulatory axis driven by NAT10 sustains proliferative signaling in colorectal cancer.Translational oncology · 2026Article
- NAT10 promotes colon cancer progression by enhancing predicted N4-acetylcytidine modification of Notch2 mRNA.Discover oncology · 2026Article
- Article
- Epitranscriptomic control of cancer: the emerging roles of m⁵C and ac⁴C RNA modifications.Cell death discovery · 2026Review
- Review
- STEAP1 Suppresses Oral Squamous Cell Carcinoma by Targeting Wnt/β-Catenin Signalling and EMT.Cancer medicine · 2026Article
- Suppressive role of SCN4B in the epithelial‑mesenchymal transition of lung adenocarcinoma.Oncology reports · 2026Article
- The NAT10/acCell communication and signaling : CCS · 2026Review
- Exploring the effects of tinzaparin and cisplatin on lung cancer cells in vitro.Cancer cell international · 2026Article
- Epitranscriptomic control of epithelial-mesenchymal transition in cancer: mechanisms, plasticity, and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Functional roles and mechanisms of NAT10-mediated RNA acFrontiers in cell and developmental biology · 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
- 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
- The function of NAT10-driven N4-acetylcytidine modification in cancer: novel insights and potential therapeutic targets.Cell & bioscience · 2025Review
- NAT10 Knockdown Improves Cisplatin Sensitivity in Non-Small Cell Lung Cancer by Inhibiting the TRIM44/PI3K/AKT Pathway.Thoracic cancer · 2025Article
- Role of NAT10-mediated acBMC pulmonary medicine · 2025Article
- Emerging Role of NAT10 as ac4C Writer in Inflammatory Diseases: Mechanisms and Therapeutic Applications.Current drug targets · 2025Review
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8 authors.
Funding
Abstract
backgroundLung cancer remains the foremost reason of cancer-related mortality, with invasion and metastasis profoundly influencing patient prognosis. N-acetyltransferase 10 (NAT10) catalyzes the exclusive N (4)-acetylcytidine (ac4C) modification in eukaryotic RNA. NAT10 dysregulation is linked to various diseases, yet its role in non-small cell lung cancer (NSCLC) invasion and metastasis remains unclear. Our study delves into the clinical significance and functional aspects of NAT10 in NSCLC.
methodsWe investigated NAT10's clinical relevance using The Cancer Genome Atlas (TCGA) and a group of 98 NSCLC patients. Employing WB, qRT-PCR, and IHC analyses, we assessed NAT10 expression in NSCLC tissues, bronchial epithelial cells (BECs), NSCLC cell lines, and mouse xenografts. Further, knockdown and overexpression techniques (siRNA, shRNA, and plasmid) were employed to evaluate NAT10's effects. A series of assays were carried out, including CCK-8, colony formation, wound healing, and transwell assays, to elucidate NAT10's role in proliferation, invasion, and metastasis. Additionally, we utilized lung cancer patient-derived 3D organoids, mouse xenograft models, and Remodelin (NAT10 inhibitor) to corroborate these findings.
resultsOur investigations revealed high NAT10 expression in NSCLC tissues, cell lines and mouse xenograft models. High NAT10 level correlated with advanced T stage, lymph node metastasis and poor overall survive. NAT10 knockdown curtailed proliferation, invasion, and migration, whereas NAT10 overexpression yielded contrary effects. Furthermore, diminished NAT10 levels correlated with increased E-cadherin level whereas decreased N-cadherin and vimentin expressions, while heightened NAT10 expression displayed contrasting results. Notably, Remodelin efficiently attenuated NSCLC proliferation, invasion, and migration by inhibiting NAT10 through the epithelial-mesenchymal transition (EMT) pathway.
conclusionsOur data underscore NAT10 as a potential therapeutic target for NSCLC, presenting avenues for targeted intervention against lung cancer through NAT10 inhibition.
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