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DNA hypomethylation restrains early antitumor immunity in prostate cancer [Nanopore]

ABSTRACT: DNA hypomethylation restrains early antitumor immunity in prostate cancer [Nanopore]

PROVIDER: PRJNA864844 | ENA |

REPOSITORIES: ENA

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DNA hypomethylation restrains early antitumor immunity in prostate cancer

Project description:DNA hypomethylation restrains early antitumor immunity in prostate cancer

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DNA hypomethylation restrains early antitumor immunity in prostate cancer [RNAseq]

Project description:DNA hypomethylation restrains early antitumor immunity in prostate cancer [RNAseq]

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DNA hypomethylation restrains early antitumor immunity in prostate cancer [DNA methylation]

Project description:DNA hypomethylation restrains early antitumor immunity in prostate cancer [DNA methylation]

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DNA hypomethylation restrains early antitumor immunity in prostate cancer [Nanopore]

Project description:Cancer is characterized by hypomethylation-associated silencing of large chromatin domains, whose contribution to tumorigenesis is uncertain. Through high-resolution single cell DNA methylation sequencing in prostate cancer, we identify 40 core hypomethylation domains, consistently hypomethylated across tumor cells and arising at early stages of malignancy. Transcriptionally silenced genes within these domains are enriched for immune-related genes; nested among repressive domains are small loci with preserved methylation, encoding cell proliferation genes that escape silencing. Prominent among hypomethylation-silenced genes is a gene cluster harboring all five CD1 genes that present lipid antigens to NKT cells, and four IFI16-related interferon-inducible genes implicated in innate immunity. Re-expression of CD1 or IFI16 murine orthologs in immunocompetent mice abrogates prostate tumorigenesis, accompanied by activation of anti-tumor immunity. Thus, early epigenetic changes in cancer may shape tumorigenesis, targeting co-located genes within defined chromosomal loci. Hypomethylation domains are detectable in blood specimens enriched for circulating tumor cells.

2023-06-14 | GSE210260 | GEO

DNA hypomethylation restrains early antitumor immunity in prostate cancer [ChIP-seq and CUT&RUN]

Project description:DNA hypomethylation restrains early antitumor immunity in prostate cancer [ChIP-seq and CUT&RUN]

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DNA hypomethylation restrains early antitumor immunity in prostate cancer [RNAseq]

2023-06-14 | GSE208448 | GEO

DNA hypomethylation restrains early antitumor immunity in prostate cancer [DNA methylation]

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Noncanonical MAVS signaling restrains dendritic cell-driven antitumor immunity by inhibiting IL-12

Project description:Noncanonical MAVS signaling restrains dendritic cell-driven antitumor immunity by inhibiting IL-12

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Noncanonical MAVS signaling restrains dendritic cell-driven antitumor immunity by inhibiting IL-12

Project description:MAVS-mediated cytosolic RNA sensing plays a central role in tumor immunogenicity. However, the effects of host MAVS signaling on antitumor immunity remains uncertain. Here, we demonstrate that host MAVS pathway drives accelerated tumor growth and impairs antitumor immunity, while MAVS knockout in dendritic cells (DCs) promotes tumor-reactive CD8+ T cell responses. Specifically, the CD8+ T cell priming capacity is enhanced by lack of functional MAVS in a type I interferon-independent, but IL-12-dependent, manner. Mechanistically, loss of RIG-I/MAVS cascade activates non-canonical NF-κB pathway and in turn induces IL-12 production by DCs, resulting in CD8+ T cell: DC crosstalk licensed by IFN-γ and IL-12. Moreover, ablation of host MAVS sensitizes tumors to immunotherapy and attenuates radiation resistance, thereby facilitating the maintenance of effector CD8+ T cells. These findings identify that host MAVS pathway acts as an immune checkpoint of DC-driven antitumor immunity, indicating the development of DC-based immunotherapies through MAVS signaling antagonism.

2023-08-15 | GSE236763 | GEO

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