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RNA-seq analysis of αPD-1 treatment outcomes in IL-34 expressing or not expressing CT26 cell line

ABSTRACT: RNA-seq analysis of αPD-1 treatment outcomes in IL-34 expressing or not expressing CT26 cell line

PROVIDER: PRJNA662114 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12605317_1.fastq.gz	Fastqsanger.gz
	SRR12605317_2.fastq.gz	Fastqsanger.gz
	SRR12605318_1.fastq.gz	Fastqsanger.gz
	SRR12605318_2.fastq.gz	Fastqsanger.gz
	SRR12605319_1.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of αPD-1 treatment outcomes in IL-34 expressing or not expressing CT26 cell line

Project description:Interleukin-34 (IL-34) is an alternative ligand to colony-stimulating factor-1 (CSF-1) for the CSF-1 receptor that acts as a key regulator of monocyte/macrophage lineage. In this study, we show that cancer cells-derived IL-34 mediates resistance to immune checkpoint blockade regardless of CSF-1 existence. In a therapeutic study of a programmed death-1 and cytotoxic T-lymphocyte-associated antigen-4 blocking monoclonal antibody, the expression of IL-34 in tumors was accompanied with limited benefits compared to IL-34 non-expressing tumors in various murine cancer models. Consistent with its immunosuppressive characteristics, the expression of IL-34 in tumors correlates with decreased frequencies of cellular (such as CD8+ and CD4+ T cells) and molecular (including various cytokines and chemokines) effectors at the tumor microenvironment. In addition, IL-34 blockade expands the M1-macrophage population. Then, a neutralizing antibody against IL-34 helped to reverse these effects and improved the therapeutic effects of the immune checkpoint blockade in combinatorial therapeutic models, including a patient-derived xenograft model of primary lung adenocarcinoma. Collectively, we revealed that tumor-derived IL-34 inhibits the efficacy of immune checkpoint blockade and proposed the utility of IL-34 blockade as a new strategy for cancer therapy.

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RNA profiling of IL-34 overexpressing acute myeloid leukemia (AML) cells

Project description:Acute myeloid leukemia (AML) is a highly heterogeneous disease. In our study, we found that overexpressing IL-34 in AML cells accelerates the AML progression and shorten the mice survival, which is medicated by LSC level. We used one of the LSC markers, c-Kit, to divide AML cells. The goals of this study aim to reveal the mechanism mediated by IL-34 overexpression, we performed the RNAseq profiling of MA9-c-kit-, MA9-c-kit+ and MA9-IL-34 AML cells.

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TCR variable regions transcripts of CT26-shppp2r1a and CT26-scr samples

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