ArticleOxidative medicine and cellular longevity2019
N-Acetyltransferase 10 Enhances Doxorubicin Resistance in Human Hepatocellular Carcinoma Cell Lines by Promoting the Epithelial-to-Mesenchymal Transition.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 60 citations in OpenAlex.
- NAT10 promotes proliferation, invasion, and epithelial-mesenchymal transition in hepatocellular carcinoma through α-tubulin acetylation.Cell adhesion & migration · 2026Article
- NAT10 drives hepatocellular carcinoma progression through SQLE-mediated cholesterol biosynthesis and is targetable by remodelin.iScience · 2026Article
- N4-acetylcytidine modification bridges metabolic reprogramming and immune evasion in cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Targeting NAT10 with Remodelin in cancer drug resistance: mechanisms, preclinical evidence, and combination strategies.Frontiers in pharmacology · 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
- NAT10 promotes glycolysis and cell stemness of ovarian cancer cells via ac4C acetylation of PGAM1 mRNA.Scientific reports · 2025Article
- NAT10-mediated N4-acetylcytidine modification in KLF9 mRNA promotes adipogenesis.Cell death and differentiation · 2025Article
- Article
- Hepatocellular carcinoma drug resistance models.Cancer cell international · 2025Review
- Single-cell imaging of N4-acetylcytidine-modified RNA using fluorine metabolic labeling mediated proximity ligation assay.Nucleic acids research · 2025Article
- Biological function and mechanism of NAT10 in cancer.Cancer innovation · 2025Review
- The N-acetyltransferase 10 inhibitor [EJNMMI radiopharmacy and chemistry · 2025Article
- Research progress on NAT10-mediated acetylation in normal development and disease.Frontiers in cell and developmental biology · 2025Review
- Review
- 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
- The role and mechanism of NAT10-mediated ac4C modification in tumor development and progression.MedComm · 2024Review
- mOncogene · 2024Article
- NAT10 inhibition promotes ac4C-dependent ferroptosis to counteract sorafenib resistance in nasopharyngeal carcinoma.Cancer science · 2024Article
- Chemotherapy-induced acetylation of ACLY by NAT10 promotes its nuclear accumulation and acetyl-CoA production to drive chemoresistance in hepatocellular carcinoma.Cell death & disease · 2024Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundN-Acetyltransferase 10 (NAT10) has been reported to be expressed at high levels in hepatocellular carcinoma (HCC); however, its role in chemoresistance is unclear. This study is aimed at investigating whether NAT10 regulates the epithelial-mesenchymal transition (EMT) and chemoresistance in HCC.
methodsHCC cell lines (Huh-7, Bel-7402, SNU387, and SNU449) were treated with remodelin, an inhibitor of NAT10, or transfected with small inhibitory RNAs (siRNAs) targeting NAT10 or Twist. The EMT was induced by hypoxia. The CCK-8 assay was used to quantify cell viability, the EdU incorporation assay to assess cell proliferation. siRNA knockdown efficiency and epithelial/mesenchymal marker expression were assessed by western blotting.
resultsKnockdown of NAT10 using siRNA or inhibition of NAT10 using remodelin increased the sensitivity of HCC cell lines to doxorubicin; similar effects were observed in cells transfected with the Twist siRNA. Inhibition of NAT10 using remodelin also reversed the ability of doxorubicin to induce the EMT in HCC cells. Furthermore, inhibiting NAT10 reversed the hypoxia-induced EMT. Finally, we confirmed that combining doxorubicin with remodelin delayed tumor growth and reduced tumor cell proliferation in a mouse xenograft model of HCC.
conclusionsNAT10 may contribute to chemoresistance in HCC by regulating the EMT. The mechanism by which NAT10 regulates the EMT and doxorubicin sensitivity in HCC cells merits further investigation.
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