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Targeting cathepsin B by cycloastragenol enhances anti-tumor immunity via inhibiting MHC-1 degradation and promoting the presentation of tumor antigen [ATAC-seq]

ABSTRACT: Targeting cathepsin B by cycloastragenol enhances anti-tumor immunity via inhibiting MHC-1 degradation and promoting the presentation of tumor antigen [ATAC-seq]

PROVIDER: PRJNA809397 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18104984_1.fastq.gz	Fastqsanger.gz
	SRR18104984_2.fastq.gz	Fastqsanger.gz
	SRR18104985_1.fastq.gz	Fastqsanger.gz
	SRR18104985_2.fastq.gz	Fastqsanger.gz

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Targeting cathepsin B by cycloastragenol enhances anti-tumor immunity via inhibiting MHC-1 degradation and promoting the presentation of tumor antigen

Project description:Targeting cathepsin B by cycloastragenol enhances anti-tumor immunity via inhibiting MHC-1 degradation and promoting the presentation of tumor antigen

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Targeting cathepsin B by cycloastragenol enhances anti-tumor immunity via inhibiting MHC-1 degradation and promoting the presentation of tumor antigen [RNA-seq]

Project description:Targeting cathepsin B by cycloastragenol enhances anti-tumor immunity via inhibiting MHC-1 degradation and promoting the presentation of tumor antigen [RNA-seq]

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Targeting cathepsin B by cycloastragenol enhances anti-tumor immunity via inhibiting MHC-1 degradation and promoting the presentation of tumor antigen [RNA-seq]

Project description:Purpose:We want to elaborate the specific mechanism of CAG inhibiting the growth of transplanted mouse colon cancer cell MC38. Methods:After MC38 cells were inoculated into C57BL/6 mice for 6 days, the mice were evenly divided into PBS group and CAG group, and PBS and CAG (50mg / kg) were administered by gavage every day. On the 18th day, the mouse tumors were removed, and one tumor was selected to prepare single cell suspension for 10x-scRNA-seq and 10x-scATAC-seq. Results:We found that CAG promoted the antigen-presenting function of tumor cells and enhanced the killing ability of CD8 T cells. Conclusions:CAG enhances the antitumor immunity of CD8 T cells by promoting the antigen presentation of tumor cells.

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Project description:Current cancer immunotherapies are assumed to improve infiltration and cytotoxicity of immune cells in the tumor. However, tumor cells have developed a variety of resistance mechanisms to suppress the MHC class I antigen presentation, and thereby impair the cytotoxicity of CD8+ T cells. Here, we identified Mal2 as a key player that mediates the turnover of the antigen-MHC-I complex and reduce the antigen presentation on tumor cells. Mal2 promotes the endocytosis of tumor antigen via direct interaction with the MHC-I complex and endosome-associated Rab5/7. In mouse and human breast tumor models, inhibition of Mal2 profoundly enhanced the cytotoxicity of tumor-infiltrating CD8+ T cells and suppressed breast tumor growth, suggesting that Mal2 is a potential target for breast cancer immunotherapy.

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Project description:Tumors frequently subvert MHC class I (MHC-I) peptide presentation to evade CD8+ T cell immunosurveillance, though how this is accomplished is not always well-defined. To identify the global regulatory networks controlling antigen presentation, we employed genome-wide screening in human diffuse large B cell lymphomas (DLBCLs). This approach revealed dozens of genes that positively and negatively modulate MHC-I cell surface expression. Validated genes clustered in multiple pathways including cytokine signaling, mRNA processing, endosomal trafficking, and protein metabolism. Genes can exhibit lymphoma subtype- or tumor-specific MHC-I regulation, and a majority of primary DLBCL tumors displayed genetic alterations in multiple regulators. We established SUGT1 as a major positive regulator of both MHC-I and MHC-II cell surface expression. Further, pharmacological inhibition of two negative regulators of antigen presentation, EZH2 and thymidylate synthase, enhanced DLBCL MHC-I presentation. These and other genes represent potential targets for manipulating MHC-I immunosurveillance in cancers, infectious diseases, and autoimmunity.

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Targeting cathepsin B by cycloastragenol enhances anti-tumor immunity via inhibiting MHC-1 degradation and promoting the presentation of tumor antigen

Project description:This SuperSeries is composed of the SubSeries listed below.

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