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Spermine Synthase Engages in Macrophages M2 polarization to Sabotage Antitumor Immunity in Hepatocellular Carcinoma (Hepa 1-6 cell)

ABSTRACT: Spermine Synthase Engages in Macrophages M2 polarization to Sabotage Antitumor Immunity in Hepatocellular Carcinoma (Hepa 1-6 cell)

PROVIDER: PRJNA1162866 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30725124_1.fastq.gz	Fastqsanger.gz
	SRR30725124_2.fastq.gz	Fastqsanger.gz
	SRR30725125_1.fastq.gz	Fastqsanger.gz
	SRR30725125_2.fastq.gz	Fastqsanger.gz
	SRR30725126_1.fastq.gz	Fastqsanger.gz

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

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

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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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Spermine Synthase Engages in Macrophages M2 polarization to Sabotage Antitumor Immunity in Hepatocellular Carcinoma (Hepa 1-6 cell)

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Spermine-induced gene expression change in human macrophages

Project description:Polyamines, crucial molecules involved in cell proliferation and growth, play a pivotal role in cancer development and progression. Within the tumor microenvironment, macrophages, key components of the immune system, exhibit a complex relationship with polyamines. Evidence suggests that polyamines can modulate macrophage polarization, influencing their functional phenotypes. Here, we detected the gene expression changes in spermine-stimulated human macrophages isolated from PBMCs.

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DSS/spermine

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Spermine-induced DNA methylation change in human macrophages

Project description:Polyamines, crucial molecules involved in cell proliferation and growth, play a pivotal role in cancer development and progression. Within the tumor microenvironment, macrophages, key components of the immune system, exhibit a complex relationship with polyamines. Evidence suggests that polyamines can modulate macrophage polarization, influencing their functional phenotypes. Here, we detected the gene DNA methylation changes in spermine-stimulated human macrophages isolated from PBMCs and TAMs.

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Cellular spermine targets JAK1 to restrain cytokine-mediated autoimmunity

Project description:Combining metabolomics analyses with an IFN-stimulated response elements reporter system, we identify spermine as a cellular metabolite brake for JAK1 signaling. Spermine directly binds to FERM and SH2 domains of JAK1 to impair IFNAR2-JAK1 interaction. Spermine suppresses JAK1 phosphorylation triggered by types I and II cytokines, including IFN-I/II, IL-2, and IL-6. Spermine treatment attenuates autoimmune pathogenesis in a SLE murine model and reduces IFN-I signaling in monocytes from SLE patients, which have reduced spermine levels.

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Cellular spermine controls autoinflammation by targeting JAK1 to restrain cytokine response

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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Project description:Analysis of gene expression profiles of HeLa cells after spermine exposure.

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