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Next Generation Sequencing was performed on MDSCs from tumors of control or alisertib treated tumor-bearing mice

ABSTRACT: Next Generation Sequencing was performed on MDSCs from tumors of control or alisertib treated tumor-bearing mice

PROVIDER: PRJNA497807 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8083882_1.fastq.gz	Fastqsanger.gz
	SRR8083882_2.fastq.gz	Fastqsanger.gz
	SRR8083883_1.fastq.gz	Fastqsanger.gz
	SRR8083883_2.fastq.gz	Fastqsanger.gz
	SRR8083884_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing was performed on MDSCs from tumors of control or alisertib treated tumor-bearing mice

Project description:The Aurora-A inhibitor alisertib shows encouraging activities in clinical trials against multiple malignances including advanced breast cancer. However, its mechanism of action remains unclear, especially regarding how the inflammatory microenvironment is involved in the efficacy of alisertib. Here, we demonstrated that Aurora-A inhibition directly reshapes the immune microenvironment through removal of tumor-promoting myeloid cells and enrichment of anti-cancer T lymphocytes, which restores a tumor-suppressive microenvironment and significantly contributes to the regression of murine mammary tumors. Mechanistically, the Aurora-A inhibitor effectively eliminated myeloid cells including myeloid-derived suppressor cells (MDSCs) and macrophages in tumors by triggering apoptosis of these cells. Further, Aurora-A inhibition could disrupt the immunosuppressive functions of MDSCs through inhibiting Stat3 mediated ROS production. These alterations led to significant increases in the proportion and the number of CD8+ and CD4+ T lymphocytes, which efficiently inhibited the proliferation of tumor cells. In summary, these data revealed that in addition to suppressing the proliferation of tumor cells, Aurora-A inhibitor directly modulates and restores an anti-tumor immune-microenvironment in breast cancer. Intriguingly, Aurora-A inactivation combined with PD-L1 blockade showed synergistic efficacy in the treatment of mammary tumors, providing an effective strategy for clinical trials of chemo-immunotherapy in breast cancer.

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Project description:Myeloid-derived suppressor cells (MDSCs) are increased by tumor-derived factors and suppress anti-tumor immunity. MDSCs obtained at a late time point after tumor injection had stronger suppressive activity than MDSCs obtained at an early time point, as measured by T cell proliferation assays. To find factors in MDSCs that change during tumor growth, we analyzed gene expression profiles from MDSCs at different time points after tumor injection. We found that immune response-related genes were down-regulated, but pro-tumor function-related genes were up-regulated in both Mo-MDSCs and PMN-MDSCs at the late time point. Among differentially expressed genes, FK506 binding protein 51 (FKBP51), which is a member of the immunophilin protein family and plays a role in immunoregulation, was increased in the Mo- and PMN-MDSCs isolated from the late time points. Experiments using siRNA and a chemical inhibitor of FKBP51 revealed that FKBP51 contributes to the regulation of the suppressive function of MDSCs by increasing iNOS, ARG1, and ROS levels and enhancing NF-kappaB activity. Collectively, our data suggest that FKBP51 is a novel molecule that can be targeted to regulate the immunosuppressive function of MDSCs. To identify the factors that licensed MDSCs to be more suppressive as tumors grow, we analyzed gene expression profiles in the two subsets of MDSCs at different time points (3wks, 6wks) during tumor progression. CD11b+Ly-6C(high)Ly-6G(low) Mo-MDSCs and CD11b+Ly-6C(low)Ly-6G(high) PMN-MDSCs were sorted from pooled spleens of naÃ¯ve mice and Her-2/CT26 tumor-bearing mice. Total RNA was purified and gene expression was analyzed by the Affymetrix GeneChipÂ® Mouse Gene 1.0 ST Array.

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Project description:Myeloid derived suppressor cells (MDSCs) are an immunosuppressive population of immature myeloid cells found in advanced stage cancer patients and mouse tumor models. To identify potential genes playing essential role in MDSC biology, we have conducted microarray analysis of gene expression in MDSCs from esophageal tumor-bearing mice, compared to immature myeloid cells from healthy littermate control mice. In this dataset, we include the expression data obtained from sorted splenic CD11b+Gr1+ cells from tumor-bearing L2-Cre;p120f/f mice, compared to healthy littermate controls. Using these data, we have identified 964 genes showing differential expression between the two groups. Among these was the Cd38 gene, which was among the genes most upregulated in MDSCs from tumor-bearing mice. 9 total samples were analyzed: 6 sample from experimental tumor-bearing mice and three pooled samples from control mice. Gene expression difference was determined by univariate test (two-sample t-test) with multivariate permutation test (10,000 random permutations). A cut-off p-value of less than 0.001 and minimum 2-fold expression change were used to identify genes with significant expression differences between the two groups.

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