ArticleiScience2025
EZH2 loss during metabolic stress drives restoration of MHC class I machinery in melanoma.
Article in iScience, 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
12 authors.
Funding
Abstract
Immune checkpoint blockade (ICB) has revolutionized metastatic melanoma care, yet many patients remain unresponsive. The tumor microenvironment (TME), shaped by metabolic stress, influences tumor antigenicity and ICB sensitivity. Here, we show that prolonged metabolic stress enhances melanoma antigen presentation via epigenetic mechanisms. Glucose-deprived melanoma cells, mimicking the nutrient-deprived TME, exhibit increased major histocompatibility complex class I (MHC-I) expression and heightened T cell-mediated killing. Proteomic and chromatin analyses reveal that metabolic stress reduces histone methyltransferase enhancer of zeste homolog 2 (EZH2), leading to H3K27me3 loss at MHC-I regulatory genes. Chromatin immunoprecipitation (ChIP) sequencing and ChIP-PCR reveal H3K27me3 loss at genes specific to MHC-I presentation. Prolonged metabolic stress transcriptionally reduces EZH2 and H3K27me3 at these promoters, elevating MHC-I antigenicity and CD8
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