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Cryoablation reshapes the immune microenvironment in the distal tumor and enhances the anti-tumor immunity

ABSTRACT: Cryoablation reshapes the immune microenvironment in the distal tumor and enhances the anti-tumor immunity

PROVIDER: PRJNA832275 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18925565_1.fastq.gz	Fastqsanger.gz
	SRR18925565_2.fastq.gz	Fastqsanger.gz
	SRR18925566_1.fastq.gz	Fastqsanger.gz
	SRR18925566_2.fastq.gz	Fastqsanger.gz
	SRR18925567_1.fastq.gz	Fastqsanger.gz

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Cryoablation reshapes the immune microenvironment in the distal tumor and enhances the anti-tumor immunity

Project description:As one of the local treatments, cryoablation plays an increasingly important role in the comprehensive treatment of malignant tumors with its advantages of less trauma, high reproducibility, and minimally invasive. Activation of anti-tumor immunity, another characteristic of cryoablation, has attracted more and more attention with the extensive application of immunotherapy. Unfortunately, the mechanism by which cryoablation enhances anti-tumor immunity is still unclear. In this study, we used a multi-omics approach to investigate the effects of local cryoablation on the distal tumor microenvironment. In this study, we proved that large amounts of tumor antigens are released post-cryoablation, leading to a sterile inflammatory response in distant tumors. During this period, lysosome-related pathways are activated, resulting in overexpression of SNAP23 and STXBP2, activation of immune effector cells, suppression of the release of immunosuppressive factors, and finally enhancement of anti-tumor immunity. Finally, cryoablation turning “Cold tumors” into “Hot tumors”, which shows a broad prospect in the combined immunotherapy.

2022-08-23 | GSE201590 | GEO

MoS2 Reshapes the Tumor Microenvironment to Promote Tumor Cell Ferroptosis

Project description:MoS2 Reshapes the Tumor Microenvironment to Promote Tumor Cell Ferroptosis

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MoS2 Reshapes the Tumor Microenvironment to Promote Tumor Cell Ferroptosis

Project description:MoS2 has found application in various biomedical fields, such as bioimaging and drug delivery. Nonetheless, utilizing MoS2 for anti-tumor therapy remains challenging, especially tumor immunotherapy. Macrophages, pivotal constituents of the tumor microenvironment, play a crucial role in driving tumor progression and chemoresistance. Modulating macrophages to reshape this microenvironment stands as a promising avenue for effective tumor treatment. In this study, we unveil a mechanism by which MoS2 induces the metamorphosis of macrophages from an M0 to an M1 phenotype, thus altering the tumor microenvironment. This transformation triggers pathways associated with inflammation within M1-type macrophages, leading to an upsurge in the expression of inflammatory molecules like IL1β. Macrophages activated by MoS2 exhibit a propensity to impede tumor cell proliferation. Through comprehensive RNA-sequencing analysis, we noted that MoS2 induces a greater enrichment of differentially expressed genes in the cytokine release pathway within macrophages. The excessive secretion of IL1β by MoS2-activated macrophages emerges as a pivotal catalyst, heightening ROS levels and decreasing GSH levels within tumor cells, ultimately culminating in ferroptosis. Therefore, we suggest MoS2 effectively reshapes the tumor microenvironment by steering macrophages toward releasing inflammatory molecules. The MoS2-triggered activation of macrophages, inducing the secretion of IL1β, emerges as a potent trigger for ferroptosis within tumor cells. Consequently, MoS2 holds substantial promise as an efficacious strategy for anti-tumor immunotherapy, achieved through the polarization of macrophages.

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Tet2 inactivation enhances the anti-tumor activity of tumor-infiltrating lymphocytes

Project description:Inactivation of tumor infiltrating lymphocytes (TILs) is one of the limiting factors of anti-tumor immunity during tumor onset and progression. Epigenetic abnormalities are regarded as a major culprit contributing to the dysfunction of TILs within tumor microenvironment. In this study, we used a murine model of melanoma to discover that Tet2 inactivation significantly enhances the anti-tumor activity of TILs, with the efficacy comparable to immune checkpoint inhibition imposed by anti-PD-L1 treatment. Single-cell RNA-seq analysis further reveals that Tet2-deficient TILs exhibit effector-like features. Transcriptomic and ATAC-seq analysis further demonstrated that Tet2 deletion reshapes the chromatin accessibility and favors the binding of transcription factors geared toward CD8+ T cell activation. In summary, our study establishes that Tet2 constitutes one of the epigenetic barriers contributing to dysfunction of TILs during anti-tumor immunity, and that Tet2 inactivation could benefit anti-tumor immunity and suppress tumor growth.

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