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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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