ArticleMedical oncology (Northwood, London, England)2026
YTHDF2 drives malignant progression in cutaneous melanoma through m⁶A-dependent HMOX1-mediated ferroptosis.
Article in Medical oncology (Northwood, London, England), 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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Abstract
N6-methyladenosine (m6A) modification plays a critical role in eukaryotic mRNA and is significantly associated with cutaneous melanoma. This study investigated the role of the m6A-binding protein YTHDF2 in the pathogenesis of cutaneous melanoma and its potential therapeutic applications. Analyses of public databases indicated that YTHDF2 exhibited elevated expression in various cancers, including cutaneous melanoma, where its levels positively correlated with PD-L1 and negatively correlated with immune and stromal scores. Functionally, the downregulation of YTHDF2 in melanoma cells suppressed proliferation and increased the population of Annexin V/PI--positive cells, an effect that was rescued by the ferroptosis inhibitor, highlighting YTHDF2's involvement in ferroptosis regulation. YTHDF2 knockdown resulted in increased intracellular Fe
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