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N4\u2010acetylcytidine (ac4C) modification, catalyzed by the <jats:italic>N<\/jats:italic>\u2010acetyltransferase 10 (NAT10), was a novel type of chemical modification that improves translation efficiency and mRNA stability.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>GEO databases and clinical samples were used to explore the expression and clinical value of NAT10 in DLBCL. CRISPER\/Cas9\u2010mediated knockout of NAT10 was performed to determine the biological functions of NAT10 in DLBCL. RNA sequencing, acetylated RNA immunoprecipitation sequencing (acRIP\u2010seq), LC\u2010MS\/MS, RNA immunoprecipitation (RIP)\u2010qPCR and RNA stability assays were performed to explore the mechanism by which NAT10 contributed to DLBCL progression.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Here, we demonstrated that NAT10\u2010mediated ac4C modification regulated the occurrence and progression of DLBCL. Dysregulated <jats:italic>N<\/jats:italic>\u2010acetyltransferases expression was found in DLBCL samples. High expression of NAT10 was associated with poor prognosis of DLBCL patients. Deletion of NAT10 expression inhibited cell proliferation and induced G0\/G1 phase arrest. Furthermore, knockout of NAT10 increased the sensitivity of DLBCL cells to ibrutinib. AcRIP\u2010seq identified solute carrier family 30 member 9 (SLC30A9) as a downstream target of NAT10 in DLBCL. NAT10 regulated the mRNA stability of SLC30A9 in an ac4C\u2010dependent manner. Genetic silencing of SLC30A9 suppressed DLBCL cell growth via regulating the activation of AMP\u2010activated protein kinase (AMPK) pathway.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Collectively, these findings highlighted the essential role of ac4C RNA modification mediated by NAT10 in DLBCL, and provided insights into novel epigenetic\u2010based therapeutic strategies.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ctm2.1747","type":"journal-article","created":{"date-parts":[[2024,7,4]],"date-time":"2024-07-04T03:45:42Z","timestamp":1720064742000},"source":"Crossref","is-referenced-by-count":18,"title":["<i>N<\/i>\u2010acetyltransferase 10 facilitates tumorigenesis of diffuse large B\u2010cell lymphoma by regulating AMPK\/mTOR signalling through N4\u2010acetylcytidine modification of SLC30A9"],"prefix":"10.1002","volume":"14","author":[{"given":"Mengfei","family":"Ding","sequence":"first","affiliation":[{"name":"Department of Hematology, Shandong Provincial Hospital Shandong University Jinan Shandong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhuoya","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Hematology, Shandong Provincial Hospital Shandong University Jinan Shandong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tiange","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Hematology, Shandong Provincial Hospital Shandong University Jinan Shandong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6893-7065","authenticated-orcid":false,"given":"Shunfeng","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of Hematology, Shandong Provincial Hospital Shandong University Jinan Shandong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiangxiang","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Hematology Shandong 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