ArticleMedical oncology (Northwood, London, England)2022
c-myc-mediated upregulation of NAT10 facilitates tumor development via cell cycle regulation in non-small cell lung cancer.
Article in Medical oncology (Northwood, London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- RNA N4-acetylcytidine modification in health and cancer: molecular mechanisms, cellular plasticity, and therapeutic opportunities.Biomarker research · 2026Review
- The functions, mechanisms and clinical relevance of RNA and protein acetyltransferase NAT10: a comprehensive review.Cell biology and toxicology · 2026Review
- RNA N4-acetylcytidine modification in human cancers: from molecular function to oncogenic mechanisms.iScience · 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
- NAT10 promotes glycolysis and cell stemness of ovarian cancer cells via ac4C acetylation of PGAM1 mRNA.Scientific reports · 2025Article
- Emerging role of N-acetyltransferase 10 in diseases: RNA ac4C modification and beyond.Molecular biomedicine · 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
- NAT10 promotes radiotherapy resistance in non-small cell lung cancer by regulating KPNB1-mediated PD-L1 nuclear translocation.Open life sciences · 2025Article
- Research progress on NAT10-mediated acetylation in normal development and disease.Frontiers in cell and developmental biology · 2025Review
- Advances of NAT10 in diseases: insights from dual properties as protein and RNA acetyltransferase.Cell biology and toxicology · 2024Review
- [Predictive Value of A miRNA Signature for Distant Metastasis in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Article
- The role and mechanism of NAT10-mediated ac4C modification in tumor development and progression.MedComm · 2024Review
- Correlation of NAT10 expression with clinical data and survival profiles in esophageal squamous cell carcinoma patients, and its impact on cell proliferation and apoptosis.Histology and histopathology · 2024Article
- NAT10/ac4C/JunB facilitates TNBC malignant progression and immunosuppression by driving glycolysis addiction.Journal of experimental & clinical cancer research : CR · 2024Article
- NAT10 and cytidine acetylation in mRNA: intersecting paths in development and disease.Current opinion in genetics & development · 2024Review
- NAT10-mediated RNA acetylation enhances HNRNPUL1 mRNA stability to contribute cervical cancer progression.International journal of medical sciences · 2023Article
- Acetyltransferase NAT10 regulates the Wnt/β-catenin signaling pathway to promote colorectal cancer progression via acJournal of experimental & clinical cancer research : CR · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
N-acetyltransferase 10 (NAT10) is a nucleolar acetyltransferase and has been reported to facilitate tumorigenesis in various cancers, but its role in NSCLC and how it is regulated remain to be assessed. The expression of NAT10 was explored in online databases and our collected clinical specimens. The relationship of NAT10 and clinical characteristics was evaluated using the online databases. Functional analyses were utilized to determine the effect of NAT10 on the proliferation and migration abilities. KEGG pathway analyses were conducted to investigate NAT10-related pathways in NSCLC. The influence of NAT10 on cell cycle was assessed by flow cytometry and cell synchronization assay. The association between c-myc and NAT10 promoter was determined by ChIP. Compared with normal tissue, NAT10 was significantly overexpressed in NSCLC. Upregulated NAT10 was associated with more advanced stage for lung adenocarcinoma and shorter overall survival and first progression time for lung cancer. NAT10 could promote proliferation and migration of NSCLC cells in vitro. c-myc positively regulated the expression of NAT10 as a transcription factor. KEGG pathway analyses indicated that NAT10 was significantly involved in cell cycle regulation, cytokine-cytokine receptor interaction and other pathways. The knockdown of NAT10-induced G1 arrest, which was possibly mediated by the downregulation of cyclin D1.Our findings suggested that c-myc-mediated upregulation of NAT10 promoted the proliferation and migration of NSCLC cells and NAT10 might be a marker for prognosis and a promising target for treatment in NSCLC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.