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

In disease-related research, NAT10 has been shown to promote cancer cell proliferation, metastasis, and apoptosis in multiple tumors. For example, in bladder cancer, NAT10 enhances cisplatin chemoresistance by promoting DNA damage repair through stabilizing AHNAK mRNA [2]. In cervical cancer, it reprograms glycolytic metabolism to promote malignancy and immunosuppression [3]. In multiple myeloma, NAT10 promotes cell proliferation by acetylating CEP170 mRNA [4]. Also, in sepsis, neutrophil-specific over-expression of NAT10 improves survival in septic mice by inhibiting neutrophil pyroptosis [5]. In periodontitis, NAT10 accelerates LPS-induced inflammation in macrophages via the NOX2-ROS-NF-κB pathway [6].

In conclusion, NAT10 is a crucial regulator in various biological processes and disease conditions. Its functions in promoting cancer progression, influencing chemoresistance, and regulating inflammatory responses and cell death in different diseases are revealed through in vivo studies including mouse models. These findings suggest that NAT10 could be a potential target for diagnosis, therapy, and prognosis in multiple clinical applications.