NAT10 REGULATES THE AMPK SIGNALING PATHWAY TO PROMOTE DLBCL PROGRESSION VIA AC4C ACETYLATION OF SLC30A9 MRNA

Introduction: N-acetyltransferase 10 (NAT10) is the only confirmed regulator to mediate N4-acetylcytidine (ac4C) modification of mRNA and crucial for stability translation efficiency. However, its role in diffuse large B-cell lymphoma (DLBCL) development prognosis has not yet been explored. Herein, we explored functional significance regulatory mechanism NAT10 mediated ac4C DLBCL, which expected propose novel therapeutic strategy. Methods: The expression levels were evaluated DLBCL cell lines lymph node biopsies tissues, prognostic value patients was further analyzed. Stable knockout constructed using CRISPR/Cas9 genomic deletion. biological functions cells analyzed vitro by proliferation cycle assays. Xenograft models used analyze effect on tumorigenesis vivo. RNA sequencing, acetylated immunoprecipitation sequencing (acRIP-seq), LC-MS/MS, RIP analyses performed explore progression. Results: upregulated tissues. high associated with poor patient prognosis. Knockout impaired cellular phase progression DLBCL. Further analysis revealed that NAT10-mediated acetylation SLC30A9 transcript subsequently stabilized mRNA, leading activation AMPK signaling thereby facilitating (Figure 1). Keywords: aggressive non-Hodgkin lymphoma, diagnostic biomarkers, genomics, epigenomics, other -omics No conflicts interests pertinent abstract.