GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE315nnn/GSE315121/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE315121GEOGSEfalseNAT10-mediated ac4C RNA acetylation stabilizes CXCL5/DEK mRNA to drive proliferation and metastasis in lung adenocarcinoma [RNA-Seq]Investigating the epigenetic mechanisms underlying lung adenocarcinoma (LUAD) through the lens of N4-acetylcytosine (ac4C) modification could innovative cancer treatment strategies and targets. 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. Moreover, NAT10 was found to significantly affect the number of metastases and tumor growth following the injection of cancer cells into the tail vein of mice. Our research data suggests that targeting NAT10 has the potential to serve as a diagnostic biomarker or prognostic target for developing anti metastatic therapies aimed at disrupting the adhesion process.2026/04/08GSE315121GSM9421695GSM942169416791315121Homo sapiens[41862454]