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TRIM27 was identified to contribute to the functional effects of IL\u20106 on skin cells. However, the underlying mechanism was not clear. Lentivirus infection was used for gene overexpression or silencing. RT\u2010PCR and Western blot were used to respectively assess mRNA and protein levels. Cell viability was assessed by CCK\u20108 assay. Extracellular flux analysis was used to assess the levels of oxygen consumption rate and extracellular acidification rate. Mouse back skin was treated with imiquimod to produce psoriasis\u2010like inflammation in\u00a0vivo. Histological assessment and immunohistochemistry staining were respectively applied to analyse lesioned mouse and human skin samples. IL\u20106\u2010induced increased viability, glycolysis and inflammation in keratinocytes was inhibited both by a chemical methylation inhibitor and by METTL14 knockdown. Further investigation found that METTL14 induces m6A methylation of TRIM27, which is recognized by a m6A reader, IGF2BP2. Elevation of TRIM27 level and activation of IL\u20106\/STAT3 signalling pathway were found in an in\u00a0vivo psoriasis\u2010like inflammation model, whereas inhibition m6A methylation strongly alleviated the inflammation. Finally, METTL14, TRIM27, STAT3, p\u2010STAT3 and IL\u20106 expressions were all found to be increased in clinical skin samples of psoriatic patients. Our results unravelled METTL14\/TRIM27\/IGF2BP2 signalling axis in keratinocyte cytopathy, which plays a critical role in facilitating the activation of IL\u20106\/STAT3 signalling pathway. Our findings should provide inspirations for the design of new therapeutics for skin inflammatory diseases including psoriasis.<\/jats:p>","DOI":"10.1111\/jcmm.18085","type":"journal-article","created":{"date-parts":[[2023,12,26]],"date-time":"2023-12-26T06:04:22Z","timestamp":1703570662000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["METTL14 promotes IL\u20106\u2010induced viability, glycolysis and inflammation in HaCaT cells via the m6A modification of TRIM27"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6765-0505","authenticated-orcid":false,"given":"Yiran","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Dermatology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine Shanghai University of Traditional Chinese Medicine  Shanghai 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