Regulatory role of IRF2 in proliferation and invasion of nasopharyngeal carcinoma and its underlying mechanism

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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Publication Details

Journal
iScience
Published
2026-07-23
DOI
https://doi.org/10.1016/j.isci.2026.116908
Primary Topic
Head and Neck Cancer Studies
Type
article
Field-Weighted Citation Impact
0.00

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article

Regulatory role of IRF2 in proliferation and invasion of nasopharyngeal carcinoma and its underlying mechanism

Xunyan Luo, Yuehua Chen, Feng Jin, Chaofen Zhao et al.
iScience
Head and Neck Cancer Studies
article

Regulatory role of IRF2 in proliferation and invasion of nasopharyngeal carcinoma and its underlying mechanism

Xunyan Luo, Yuehua Chen, Feng Jin, Chaofen Zhao, Jiayu Song
article en

Abstract

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.

iScienceVol. 29(8)
Guiyang Medical University (CN), Guizhou Cancer Hospital (CN), Affiliated Hospital of Guizhou Medical University (CN), Qiannan Normal College For Nationalities (CN)
National Natural Science Foundation of China, Science and Technology Program of Guizhou Province
Openalex Percentile: Top 7%
Head and Neck Cancer Studies
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