NAT10, or N-Acetyltransferase-like protein 10, is an enzyme with acetyltransferase and RNA-binding activities. It is the first identified enzyme to catalyze the production of N4-acetylcytidine (ac4C) in eukaryotic RNA. The ac4C modification mediated by NAT10 is involved in various biological processes such as mRNA stability, translation efficiency, oocyte maturation, bone remodeling, and fatty acid metabolism [1].

In disease-related studies, NAT10 has been shown to play significant roles. In multiple tumors, NAT10 promotes proliferation, metastasis, and apoptosis. For example, in bladder cancer, NAT10-mediated ac4C modification enhances DNA damage repair, leading to cisplatin chemoresistance [2]. In cervical cancer, the NAT10/ac4C/FOXP1 axis reprograms glycolytic metabolism, promoting malignant progression and immunosuppression [3]. In multiple myeloma, NAT10 promotes cell proliferation by acetylating CEP170 mRNA [4]. In contrast, in sepsis, down-regulation of NAT10 in neutrophils exacerbates pyroptosis via the ULK1-STING-NLRP3 axis [5].

In conclusion, NAT10 is a crucial regulator in various biological processes and diseases. Studies, especially those using loss-of-function models, have revealed its diverse roles in promoting tumor progression, influencing immune-related responses in diseases like sepsis, and affecting cardiac remodeling. These findings suggest that NAT10 could be a potential target for diagnosis, therapy, and prognosis in multiple clinical applications.