ArticleJournal of dental sciences2026
APOBEC3B/ASF1B-TGF-β signaling axis promotes epithelial-mesenchymal transition in HPV-positive oropharyngeal cancer.
Article in Journal of dental sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
Background/purpose: Human papillomavirus (HPV)-positive oropharyngeal cancer (OPC) generally shows better outcomes, yet a subset of patients develops aggressive lymphatic metastasis. The molecular determinants of this divergence remain unclear. This study explored the apolipoprotein B mRNA editing enzyme catalytic subunit 3B (APOBEC3B)/anti-silencing function 1B histone chaperone (ASF1B) axis as a potential mediator linking human papillomavirus (HPV) infection, DNA damage, and transforming growth factor beta (TGF-β) signaling in OPC. Materials and methods: Transcriptomic and clinical datasets from The Cancer Genome Atlas (TCGA) were analyzed to examine correlations among APOBEC3B/ASF1B expression, HPV status, and TGF-β signaling activity. Functional assays using HPV-positive and HPV-negative cell models assessed APOBEC3B/ASF1B expression, replication protein A2 (RPA2) activation, and epithelial-mesenchymal transition (EMT) markers through quantitative polymerase chain reaction (qPCR), western blotting, and immunofluorescence. Results: HPV infection markedly enhanced APOBEC3B and ASF1B expression, accompanied by RPA2 upregulation and EMT features. Silencing APOBEC3B reduced RPA2 and ASF1B levels and suppressed TGF-β signaling. Conclusion: These findings identify APOBEC3B/ASF1B as a central pathway through which HPV infection activates TGF-β signaling and promotes EMT, offering potential biomarkers and therapeutic targets for high-risk HPV-positive OPC.
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