ArticleCell death & disease2025
TRIM63/IRF-8 axis promotes tumor progression and immunosuppression of melanoma with BRAF mutation.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- IRF8 Suppresses Hepatocellular Carcinoma Progression Through LIAS-Dependent IFN Production and Cuproptosis Activation.Genes, chromosomes & cancer · 2026Article
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Authors and funding
6 authors.
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Abstract
The E3 ligase TRIM63 demonstrates a robust correlation with melanoma malignancy, particularly in cases involving BRAF mutants. Meanwhile, BRAF mutants, such as V600E, represent a prominent mutation observed in melanoma patients, yet the underlying mechanism remains elusive. In this study, we demonstrate that TRIM63 exhibits overexpression in melanoma cells and exerts its full oncogenic potential upon activation of the MAPK signaling pathway. Mechanistically, BRAF mutation induces ERK1/2-mediated phosphorylation of TRIM63 at serine 69 (S69). TRIM63 S69 is localized in the RING domain, and its phosphorylation enhances TRIM63 binding with IRF-8. Subsequently, TRIM63 leads to the ubiquitination of IRF-8 at lysine 250 (K250). The degradation of IRF-8 ultimately contributes to tumor progression enhancement. Clinically, the presence of pS69 on TRIM63 is associated with tumor immunosuppression and poor prognosis among melanoma patients, highlighting its potential as a promising therapeutic target.
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