Histone ChIP-Seq of B16-F10 melenoma cell lines (mouse)
In this study, we examine the impact of metabolic adaptation induced by prolonged glucose deprivation, as found in the TME, on MHC-I presentation and overall immunogenicity of melanoma cells. ChIP sequencing reveals H3K27me3 reduction at MHC-I genes during prolonged metabolic stress. We find that metabolic adaptation of melanoma cells results in loss of EZH2, restoration of MHC-I expression and antigen presentation, and an increase in T cell mediated tumor killing. Here we provide H3K27me3 ChIP-Seq for B16-F10 melanoma mouse cell line cultured under 2 conditions; normal glucose and no glucose replaced with galactose.