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Here, this study reports that <jats:italic>EBV\u2010miR\u2010BART18\u20103p<\/jats:italic> is highly expressed in colorectal cancer (CRC) and is closely associated with the pathological and advanced clinical stages of CRC. Ectopic expression of <jats:italic>EBV\u2010miR\u2010BART18\u20103p<\/jats:italic> leads to increased migration and invasion capacities of CRC cells in vitro and causes tumor metastasis in vivo. Mechanistically, <jats:italic>EBV\u2010miR\u2010BART18\u20103p<\/jats:italic> activates the hypoxia inducible factor 1 subunit alpha\/lactate dehydrogenase A axis by targeting Sirtuin, which promotes lactate accumulation and acetyl\u2010CoA production in CRC cells under hypoxic condition. Increased acetyl\u2010CoA utilization subsequently leads to histone acetylation of fatty acid synthase and fatty acid synthase\u2010dependent fat synthesis, which in turn drives de novo lipogenesis. The oncogenic role of <jats:italic>EBV\u2010miR\u2010BART18\u20103p<\/jats:italic> is confirmed in the patient\u2010derived tumor xenograft mouse model. Altogether, the findings define a novel mechanism of <jats:italic>EBV\u2010miR\u2010BART18\u20103p<\/jats:italic> in CRC development through the lipogenesis pathway and provide a potential clinical intervention target for CRC.<\/jats:p>","DOI":"10.1002\/advs.202202116","type":"journal-article","created":{"date-parts":[[2022,10,28]],"date-time":"2022-10-28T23:20:32Z","timestamp":1666999232000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Epstein\u2013Barr Virus\u2010Encoded <i>MicroRNA\u2010BART18\u20103p<\/i> Promotes Colorectal Cancer Progression by Targeting De Novo Lipogenesis"],"prefix":"10.1002","volume":"9","author":[{"given":"Qingtao","family":"Meng","sequence":"first","affiliation":[{"name":"Beijing Key Laboratory of Environmental Toxicology, School of Public Health Capital Medical University  Beijing 100069 P. R. China"},{"name":"Department of Oncology Capital Medical University  Beijing 100069 P. R. 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