TY  - JOUR
T1  - Multidimensional Pan-cancer Analysis of NAT10: Cancer-type-specific Clinical and Biological Associations and Prognostic Potential 
AU  - Ding, Yuan
AU  - Ren, Lihua
AU  - Shi, Ruihua
JF  - Cancer Screening and Prevention
VL  - 
IS  - 000
SN  - 2835-3315
SP  - 
EP  - 
Y1  - 2026-12-30
DO  - 10.14218/CSP.2026.00017
UR  - https://www.xiahepublishing.com/2835-3315/CSP-2026-00017
AB  - Background and objectives 
N-acetyltransferase 10 (NAT10), a major RNA acetyltransferase mediating N4-acetylcytidine modification, has been implicated in cancer progression. We examined its cancer-type-specific associations with clinical outcomes, genomic features, and tumor immune characteristics.
Methods
We analyzed public TCGA and GTEx datasets using UCSC Xena and complementary resources, including GEPIA2, HPA, cBioPortal, TIMER2.0, STRING, LinkedOmics, and CancerSEA. Analyses included NAT10 expression, pathological stage, survival, genomic alterations, immune-cell infiltration, stemness, and molecular pathways. Exploratory immune-checkpoint-blockade (ICB) survival analyses used Kaplan–Meier Plotter cohorts receiving anti-PD-1 (n = 411), anti-PD-L1 (n = 459), or anti-CTLA-4 (n = 112).
Results
NAT10 expression was elevated in multiple cancer types and was associated with adverse survival in selected malignancies. Higher NAT10 expression correlated positively with estimated myeloid-derived suppressor cell and cancer-associated fibroblast infiltration and negatively with several T-cell and natural killer-cell populations. NAT10-associated genes were enriched in RNA-processing pathways. In exploratory ICB cohorts, higher NAT10 expression was nominally associated with longer overall survival following anti-PD-1 therapy (hazard ratio (HR) = 0.68, 95% confidence interval (CI): 0.52–0.90) and anti-PD-L1 therapy (HR = 0.72, 95% CI: 0.56–0.92), but not anti-CTLA-4 therapy (HR = 0.66, 95% CI: 0.39–1.11).
Conclusions
NAT10 shows cancer-type-dependent prognostic, molecular, and immune associations. Its associations with survival after ICB are exploratory and require independent clinical and mechanistic validation.