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Reveals that IRF2 influences cancer cell growth in nasopharyngeal carcinoma, suggesting a new treatment target.
IRF2 is an interferon regulatory factor with context-dependent roles in cancer. We examined IRF2 expression and function in nasopharyngeal carcinoma (NPC) using immunohistochemistry, immunofluorescence, western blot, and functional assays in cell lines and a xenograft model. IRF2 was upregulated and predominantly nuclear in NPC, correlating with advanced T stage and higher EBV DNA load. ROC analysis indicated diagnostic value (AUC = 0.837). IRF2 overexpression promoted proliferation, migration, invasion, epithelial-mesenchymal transition (EMT) and suppressed apoptosis, whereas knockdown inhibited these phenotypes and reduced tumor growth in vivo . Mechanistically, IRF2 activated the Wnt/β-catenin pathway by upregulating β-catenin and facilitating its nuclear translocation. These findings establish IRF2 as an oncogenic driver in NPC and suggest the IRF2/Wnt/β-catenin axis as a potential therapeutic target.
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Zhao et al. (2026) studied this question.
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