NAT10-mediated ac4C-modified genes predict tumor prognosis and immune response in colon adenocarcinoma.

N-4 cytidine acetylation (ac4C), facilitated by N-acetyltransferase 10 (NAT10), is essential in regulating mRNA stability, rRNA biogenesis, cell proliferation, and epithelial-mesenchymal transition. However, the prognostic implications of NAT10-mediated ac4C modifications in colon adenocarcinoma (COAD) remains unclear. Our study demonstrated that NAT10 facilitates tumor growth and modulates an immune response in COAD. Moreover, we identified 2156 ac4C-related genes from the literature and obtained COAD patient information from TCGA. We constructed a prognostic risk model based on NAT10-mediated ac4C-related genes, thoroughly examining biological pathways, immune infiltration, tumor mutation burden, and drug sensitivity. The NAT10-related genes risk model developed in this study accurately predicts clinical outcomes in COAD, offering potential prognostic biomarkers and therapeutic targets. It helps identify candidates for immune checkpoint inhibitors (ICIs) and targeted therapies, offering insights for personalized precision treatment of COAD.