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The following is a summary of “Role of NAT10-mediated ac4C acetylation of ENO1 mRNA in glycolysis and apoptosis in non-small cell lung cancer cells,” published in the February 2025 issue of BMC Pulmonary Medicine by Yuan et al.
Researchers conducted a retrospective study to analyze the role of N-acetyltransferase 10 (NAT10) in non-small cell lung cancer (NSCLC) and its underlying mechanism.
They utilized reverse transcription-quantitative polymerase chain reaction and Western blot to estimate NAT10 levels in NSCLC cell lines. Cell viability, proliferation, and apoptosis in A549 and PC9 cell lines were evaluated using cell counting kit-8, colony formation assay, and flow cytometry. N4-acetylcytidine (ac4C)-RNA immunoprecipitation assay was conducted to assess ac4 C levels of α-enolase (ENO1) mRNA in A549 and PC9 cell lines. The interaction between NAT10 and ENO1 was examined through a dual-luciferase reporter assay.
The results showed that NAT10 expression was elevated in NSCLC cell lines. In A549 and PC9 cell lines, ac4 C levels of ENO1 mRNA decreased following NAT10 inhibition. Suppressing NAT10 reduced cell viability and glycolysis while increasing apoptosis in A549 and PC9 cell lines. These effects were reversed when ENO1 was overexpressed.
Investigators concluded that NAT10 regulated glycolysis and apoptosis in NSCLC through ac4 C acetylation of ENO1, potentially offering new avenues for the clinical treatment of NSCLC.
Source: bmcpulmmed.biomedcentral.com/articles/10.1186/s12890-024-03463-2
