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0This research article investigates the oncogenic role of the m6A RNA reader protein YTHDF3 in promoting cervical cancer driven by high-risk human papillomavirus (HPV). Through multi-omics analysis and gene-editing techniques, the study identifies a novel YTHDF3/STAT3/IRF7 axis that facilitates viral persistence and tumor growth. The authors demonstrate that YTHDF3 stabilizes STAT3 mRNA, which subsequently suppresses the expression of interferon-stimulated genes (ISGs) and reduces IFN-α production. This molecular signaling cascade effectively weakens the body's antiviral immunity and fosters an immunosuppressive tumor microenvironment by recruiting regulatory T cells and M2 macrophages. Ultimately, the findings suggest that inhibiting YTHDF3 could serve as a viable therapeutic strategy to restore immune surveillance and combat HPV-associated malignancies.
References:
Li L, Lin D, Ao K, et al. YTHDF3 suppresses interferon-stimulated gene (ISG)-dependent antitumor immunity and promotes HPV carcinogenesis in cervical cancer[J]. Cell Death & Disease, 2025, 17(1): 60.
