NAT10-mediated ac4C RNA acetylation stabilizes CXCL5/DEK mRNA to drive proliferation and metastasis in lung adenocarcinoma [RIP-Seq]

We used biological information methods to analyze shared data, with a focus on studying N-acetyltransferase 10 (NAT10), which is the only known ac4C "writer" protein. Our analysis revealed a significant upregulation of NAT10 expression in LUAD, a finding that was corroborated by investigations in both LUAD cancer tissue samples and cell lines.

Subsequently, we employed CRISPR/Cas9 technology to knock out the NAT10 gene and analyzed the resulting knockout cells using acRIP-seq and RNA-seq techniques. Our findings demonstrated differential expression of the genes CXCL5 and DEK, and functional enrichment analysis indicated a strong association with the adhesion signaling pathway. Laboratory experiments revealed that NAT10 acts as an ac4C "writer," promoting the acetylation of CXCL5 and DEK and thus preventing the degradation of their mRNAs.