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Myeloid-derived suppressor cells facilitie invasion and metastasis of papillary thyroid cancer cells by repressing miR-486-3p

ABSTRACT: Background：In present study, we aimed to evaluate the level as well as function of circulating MDSCs in papillary thyroid cancer (PTC), and also explore the underlying mechanism of MDSCs during tumor progression. Methods：microRNA arrays and RNA-seq analysis were conducted to screened out differentially expressed miRNAs and mRNAs between TPC-1 cells cocultured with PMN-MDSCs and untreated TPC-1 cell line. Results：19 miRNAs were differentially expressed, of which 10 were downregulated and 9 were upregulated in MDSC-conditioned cancer cells. GO analysis of miRNA predicted target genes showed that inflammatory related response were enriched. Besides, these genes were mainly related to NF-kappa B, PI3K-AKT and TNF signaling pathways which are associated with immune response as well as cancer development by KEGG pathway analysis. For validation, qRT-PCR was used to assess the differentially expressed miRNA and the trends in the expression was consistent between microRNA-seq and qRT-PCR. Conclusion：Collectively, our work explore the mechanism by which PMN-MDSCs paly a critical role in PTC

ORGANISM(S): Homo sapiens

PROVIDER: GSE140109 | GEO | 2019/11/08

REPOSITORIES: GEO

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Project description:Myeloid-derived suppressor cells (MDSCs) are key players in immune evasion, tumor progression and metastasis. MDSCs accumulate under various pathological states, and fall into two functionally and phenotypically distinct subsets: polymorphonuclear (PMN)-MDSCs and monocytic (M)-MDSCs. These subsets have been studied extensively in humans and mice, yet to date no study has identified MDSC subsets in dogs with spontaneous tumors. As dogs are an excellent model for human tumor development and progression, we set out to identify PMN-MDSCs and M-MDSCs in clinical canine oncology patients. We identified MDSCs as hypodense MHC class II-CD5-CD21-CD11b+ cells and show for the first time that they can also be subdivided into polymorphonuclear (CADO48A+CD14-) and monocytic (CADO48A-CD14+) subsets. The transcriptomic signatures of PMN-MDSCs and M-MDSCs are distinct from each other and from those of conventional polymorphonuclear (PMN) and monocytic cells, respectively. Notably, bioinformatic analyses reveal a statistically significant similarity between canine and previously published human MDSC gene expression patterns. As in humans, peripheral blood frequencies of canine PMN-MDSCs and M-MDSCs are significantly different in dogs with cancer compared to healthy control dogs (PMN-MDSCs: p < .001; M-MDSCs: p < .01). Furthermore, a comparison of our canine MDSC RNA-seq data with transcriptomic results previously published for human and murine MDSCs highlights five commonly upregulated genes in PMN-MDSCs in all species, suggesting that these genes are evolutionarily conserved and functionally important. Interestingly, one gene has previously been implicated in PMN-MDSC function (MMP8), but four genes (LTF, LCN2, CAMP, EBP41L3) are novel in the context of PMN-MDSCs. Our findings therefore demonstrate for the first time that dogs have two distinct populations of MDSCs, characterized by specific phenotypic and transcriptomic signatures that share key features of human MDSC subsets. Importantly, by leveraging the power of evolution, we have identified additional conserved genes in PMN-MDSCs of multiple species which may play a role in MDSC function. Our findings therefore validate the dog as a model for studying MDSCs in the context of cancer.

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Myeloid-derived suppressor cells facilitie invasion and metastasis of papillary thyroid cancer cells by repressing miR-486-3p

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