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.

本研究旨在探究肿瘤微环境（Tumor Microenvironment, TME）中存在的长期葡萄糖剥夺所诱导的代谢适应，对黑色素瘤细胞的主要组织相容性复合体I类（Major Histocompatibility Complex class I, MHC-I）抗原呈递及整体免疫原性的影响。染色质免疫沉淀测序（Chromatin Immunoprecipitation sequencing, ChIP-Seq）结果显示，在长期代谢应激过程中，MHC-I基因位点的组蛋白H3赖氨酸27三甲基化（Histone H3 Lysine 27 Trimethylation, H3K27me3）水平显著降低。本研究发现，黑色素瘤细胞的代谢适应会导致zeste同源物增强子2（Enhancer of Zeste Homolog 2, EZH2）表达缺失，恢复MHC-I的表达与抗原呈递能力，并增强T细胞介导的肿瘤杀伤效应。本数据集包含B16-F10小鼠黑色素瘤细胞系在两种培养条件下的H3K27me3 ChIP-Seq数据：正常葡萄糖培养组，以及无葡萄糖且以半乳糖替代的培养组。