{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T21:29:44Z","timestamp":1792099784766,"version":"4.4.0"},"reference-count":44,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T00:00:00Z","timestamp":1772150400000},"content-version":"vor","delay-in-days":57,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Breast Journal"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:p>The transcription factor c\u2010Myc is often overexpressed in chemotherapy\u2010resistant triple\u2010negative breast cancer (TNBC). c\u2010Myc function and stability are considered key factors regulating chemoresistance. Recent studies have revealed a potential link between the O\u2010linked \u03b2\u2010N\u2010acetylglucosamine modification (O\u2010GlcNAcylation) of c\u2010Myc and its function and stability; however, the underlying mechanisms remain unexplored. This study aimed to investigate the role of O\u2010GlcNAcylation in promoting chemoresistance and to explore the underlying mechanisms. A cisplatin (DDP)\u2010resistant MDA\u2010MB\u2010231\u2009cell line was established using a dose escalation. CCK\u20108, flow cytometry, and colony formation assays were used to evaluate cell resistance under different treatments. Western blotting and coimmunoprecipitation analyses were performed to evaluate the expression of c\u2010Myc and its O\u2010GlcNAcylation under different conditions. The possible O\u2010GlcNAcylation sites were predicted using DictyOGlyc 1.1. Inhibition of O\u2010linked N\u2010acetylglucosamine transferase (OGT) significantly suppressed colony formation and promoted apoptosis of DDP\u2010resistant cells. c\u2010Myc expression was downregulated when OGT\u2010mediated O\u2010GlcNAcylation was inhibited. Additionally, OGT interacted with c\u2010Myc, promoting its stability at the Thr58 residue. Mutation of Thr58 not only resulted in lower c\u2010Myc stability, reduced colony formation ability, and increased apoptosis but also resulted in a decrease in both the total expression and O\u2010GlcNAcylation of c\u2010Myc. Therefore, O\u2010GlcNAcylation at Thr\u201058 regulates c\u2010Myc activity to promote chemoresistance of TNBC cells.<\/jats:p>","DOI":"10.1155\/tbj\/2120017","type":"journal-article","created":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T23:51:50Z","timestamp":1773013910000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["OGT\u2010Mediated O\u2010GlcNAcylation Stabilizes c\u2010Myc Activity and Promotes Chemoresistance in Triple\u2010Negative Breast 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