ArticleDiscover oncology2025
Acetyltransferase NAT10 promotes gastric cancer progression by regulating the Wnt/β-catenin signaling pathway and enhances chemotherapy resistance.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- 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
- NAT10: a potential factor to reverse tumor chemotherapy resistance and radioresistance (Review).Frontiers in immunology · 2026Review
- A New Look at the Role of Radiation-Related Epigenetic Mechanisms in Diagnosis and Anticancer Therapies.Cells · 2025Review
- Targeting the Wnt/β-catenin pathway and epithelial-mesenchymal transition in gastric cancer: mechanisms, therapeutic strategies, and clinical challenges.Frontiers in oncology · 2025Review
- Silencing CDH17 reverses cisplatin resistance in gastric cancer cells by regulating the Warburg effect mediated by the Wnt/β-catenin pathway.American journal of translational research · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundN-acetyltransferase 10 (NAT10) is involved in several cellular processes. NAT10 expression is essential for the promotion of mRNA translation and stability. In some situations, deregulation of NAT10 has been attributed to the development of multiple types of cancer. NAT10 is significantly upregulated in various gastrointestinal tumors, including esophageal, colorectal, pancreatic, and liver cancers, and is correlated with poor prognosis. Additionally, NAT10 expression contributes to chemotherapy resistance in both esophageal and colorectal cancers. Nevertheless, the role of NAT10 in gastric cancer (GC), a type of gastrointestinal tumor, is not fully understood.
methodsThroughout this investigation, our team evaluated NAT10 expression levels in GC patient samples and databases available to the general public. Based on the knockdown and overexpression of NAT10, in vitro experiments were conducted to examine the effects of NAT10 on GC progression and resistance to chemotherapy.
resultsOur study demonstrated that GC tissues exhibit increased levels of NAT10. Downregulation of NAT10 decreased GC cell proliferation, migration, and invasiveness. Conversely, upregulation of NAT10 resulted in the opposite effect. Furthermore, NAT10 fosters the progression of GC cells by activating the Wnt/β-catenin signaling pathway. NAT10 also promotes resistance to cisplatin chemotherapy.
conclusionsOur findings indicated that expression of NAT10 promoted GC progression through activation of the Wnt/β-catenin signaling pathway. We investigated the effect of NAT10 on the viability of GC cells treated with different doses of cisplatin. The results showed that NAT10 expression could impact the effectiveness of chemotherapy resistance in GC. This implies that using NAT10 as a target may be a potential therapeutic strategy for treating GC.
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