Background
Abnormal expression of N-acetyltransferase 10 (NAT10) has been shown to promote the progression of various tumors, including non-small cell lung cancer (NSCLC). This study was designed to investigate the role of NAT10 in NSCLC and the underlying mechanism.
Conclusions
NAT10 regulated glycolysis and apoptosis in NSCLC via ac4C acetylating ENO1, which might provide new ideas for the clinical treatment of NSCLC.
Methods
Reverse transcription-quantitative polymerase chain reaction and Western blot were used to analyze the levels of NAT10 in NSCLC cell lines. The cell viability, proliferation, and apoptosis of A549 and PC9 cell lines were detected by cell counting kit-8, colony formation, and flow cytometry. N4-acetylcytidine (ac4C)-RNA immunoprecipitation assay was performed to detect the level of ac4C of α-enolase (ENO1) mRNA in A549 and PC9 cell lines. The relationship between NAT10 and ENO1 was performed by dual-luciferase reporter assay.
Results
NAT10 was increased in NSCLC cell lines. The ac4C level of ENO1 mRNA in A549 and PC9 cell lines was downregulated after NAT10 inhibition. Knockdown of NAT10 inhibited cell viability and glycolysis and promoted cell apoptosis in A549 and PC9 cell lines, and the results were reversed after ENO1 overexpressing. Conclusions: NAT10 regulated glycolysis and apoptosis in NSCLC via ac4C acetylating ENO1, which might provide new ideas for the clinical treatment of NSCLC.