NAT10 promotes prostate cancer progression by acetylating mRNA of MARK2 and activating mTOR/HIF-1α/C-Myc pathway to enhance glycolytic reprogramming.
Mechanistic investigations demonstrated that NAT10 elevates MARK2 expression, activating the mTOR/HIF-1α/C-Myc signaling cascade, thereby promoting aerobic glycolysis in PCa cells, suggesting that targeting ac4C mRNA modifications may provide a novel therapeutic strategy for managing prostate cancer.