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Spermine-induced gene expression change in human macrophages

ABSTRACT: Spermine-induced gene expression change in human macrophages

PROVIDER: PRJNA1108626 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28926161_1.fastq.gz	Fastqsanger.gz
	SRR28926161_2.fastq.gz	Fastqsanger.gz
	SRR28926162_1.fastq.gz	Fastqsanger.gz
	SRR28926162_2.fastq.gz	Fastqsanger.gz

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Spermine-induced DNA methylation change in human macrophages

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Spermine Synthase Engages in Macrophages M2 polarization to Sabotage Antitumor Immunity in Hepatocellular Carcinoma

Project description:Disturbances in tumor cell metabolism reshape the tumor microenvironment (TME) and impair antitumor immunity, but the implicit mechanisms remain elusive. Here, we found that spermine synthase (SMS) was significantly upregulated in tumor cells, which correlated positively with immunosuppressive microenvironments and predicted poor survival in hepatocellular carcinoma (HCC) patients. Via “subcutaneous” and “orthotopic” HCC syngeneic mouse models and a series of in vitro coculture experiments, we identified elevated SMS level in HCC cells played a role in immune escape mainly through its metabolic product spermine, which induced tumor-associated macrophage (TAM) reprogramming and subsequently corresponded with a decreased antitumor functionality of CD8+ T cells. Mechanistically, we discovered that spermine reprogrammed TAM mainly by activating the PI3K-Akt-mTOR-S6K signaling pathway. Spermine inhibition in combination with immune checkpoint blockade effectively diminishes tumor burden in vivo. Our results expand the understanding of the critical role of metabolites in regulating cancer progression and anti-tumor immunity, and open new avenues for developing novel therapeutic strategies against HCC.

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Project description:Using an unbiased metabolomics approach and a IFN-stimulated response elements (ISRE) reporter screening system, we have identified the cellular metabolite spermine as an endogenous brake restraining IFN-I signaling and autoinflammation. Cellular spermine concentration decrease upon stimulations with IFN-I, IL-2, and IL-6. Spermine suppresses phosphorylation of JAK1 in macrophages responding to IFN-I, T cells responding to IL-2, and fibroblasts responding to IL-6. Mechanistically, spermine binds directly to the N-terminal domains of JAK1, resulting in impaired IFNAR2-JAK1 interaction required for initiating downstream signaling and, subsequently, restrained IFN-I effector response. Moreover, spermine attenuates SLE progression in an SLE murine model and reduces IFN-I signaling in PBMCs from SLE patients.

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