{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T19:14:17Z","timestamp":1793819657680,"version":"4.6.1"},"reference-count":57,"publisher":"Wiley","issue":"28","license":[{"start":{"date-parts":[[2024,5,20]],"date-time":"2024-05-20T00:00:00Z","timestamp":1716163200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The RNA modification, 5\u2010methylcytosine (m\n                    <jats:sup>5<\/jats:sup>\n                    C), has recently gained prominence as a pivotal post\u2010transcriptional regulator of gene expression, intricately intertwined with various tumorigenic processes. However,\u00a0the exact mechanisms governing m\n                    <jats:sup>5<\/jats:sup>\n                    C modifications during the onset and progression\u00a0of colorectal cancer (CRC) remain unclear. Here, it is determined that the m\n                    <jats:sup>5<\/jats:sup>\n                    C methyltransferase NSUN2 exhibits significantly elevated expression and exerts an oncogenic function in CRC. Mechanistically, NSUN2 and YBX1 are identified as the \u201cwriter\u201d and \u201creader\u201d of ENO1, culminating in the reprogramming of the glucose metabolism and increased production of lactic acid in an m\n                    <jats:sup>5<\/jats:sup>\n                    C\u2010dependent manner. The accumulation of lactic acid derived from CRC cells, in turn, activates the transcription of NSUN2 through histone H3K18 lactylation (H3K18la), and induces the lactylation of NSUN2 at the Lys356 residue (K356), which is crucial for capturing target RNAs. Together,\u00a0these findings reveal an intriguing positive feedback loop involving the NSUN2\/YBX1\/m\n                    <jats:sup>5<\/jats:sup>\n                    C\u2010ENO1 signaling axis, thereby bridging the connection between metabolic reprogramming and epigenetic remodeling, which may shed light on the therapeutic potential of combining an NSUN2 inhibitor with immunotherapy for CRC.\n                  <\/jats:p>","DOI":"10.1002\/advs.202309840","type":"journal-article","created":{"date-parts":[[2024,5,21]],"date-time":"2024-05-21T00:40:46Z","timestamp":1716252046000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":148,"title":["Metabolic Recoding of NSUN2\u2010Mediated m\n                    <sup>5<\/sup>\n                    C Modification Promotes the Progression of Colorectal Cancer via the NSUN2\/YBX1\/m\n                    <sup>5<\/sup>\n                    C\u2010ENO1 Positive Feedback 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