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Deltex E3 ubiquitin ligase 3L (DTX3L) is a well-established ubiquitin ligase implicated in various cancers, but its role in nasopharyngeal carcinoma (NPC) progression remains elusive. In this study, we confirmed for the first time that DTX3L was highly expressed in C666-1 and NPC/HK1 NPC cells. DTX3L overexpression promoted NPC cell proliferation, invasion, and migration. Conversely, DTX3L knockdown suppressed these malignant phenotypes. Notably, DTX3L activated the β-catenin pathway, as evidenced by increased β-catenin nuclear translocation, increased transcriptional activity, and elevated expression of its downstream target c-Myc. Mechanistically, we identified an upstream regulatory axis in which the oncogenic long noncoding RNA H19 acted as a molecular sponge for miR-423-5p, thereby alleviating the miR-423-5p-mediated repression of DTX3L. Dual-luciferase reporter assays confirmed that miR-423-5p directly targeted both DTX3L and H19, supporting the presence of a competitive endogenous RNA (ceRNA) network. Furthermore, rescue experiments demonstrated that DTX3L knockdown largely abolished the proliferative advantage conferred by H19 overexpression. Collectively, the results of our study revealed that the H19/miR-423-5p/DTX3L axis is a novel ceRNA-driven mechanism that promotes NPC progression via activation of β-catenin signaling.