Expression data from parental B16F0 cells and B16F0 exosomes
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ABSTRACT:
PROVIDER: PRJNA399519 | ENA |
REPOSITORIES: ENA
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Project description:As a type of secreted membrane vesicle, exosomes are emerging as an important mode of cell-to-cell communication. The objective of this study was to compare the abundance of transcripts present in the parental B16F0 cell to transcripts present in exosomes isolated from B16F0 conditioned media. Identifying local mechanisms of immunosuppression is a key barrier for expanding the clinical benefit of cancer immunotherapy. While exosomes are emerging as a new mode of intercellular communication, their role in establishing a malignant tissue niche remains unclear. Similar to the sculpting of tumor antigens during oncogenesis, a related hypothesis is that proteins secreted by malignant cells are shaped by somatic evolution. To test this hypothesis, we characterized the biological influence of tumor-derived exosomes on immune cell function. In particular, we analyzed exosomes from three melanoma models: B16F0, a non-immunogenic model of malignant melanoma; Cloudman S91, a model of immunogenic melanoma; and Melan-A, an immortalized melanocyte cell line. Using electron microscopy, exosomes derived from all three cell lines were morphologically similar. The exosomes contained receptors derived from the parent cell as demonstrated by IL12RB2 expression on B16F0 exosomes and intact mRNAs. Furthermore, transcript profiling of B16F0 exosomes and cells suggested that exosomal mRNA is enriched for mRNAs that target immune-related pathways, including Ptpn11 that inhibited T cell proliferation and Dnmt3a that inhibited T cell production of IFN-gamma. Functionally, B16F0 exosomes dose-dependently suppressed cell proliferation and the expression of IL12RB2 in primary CD8+ T cells. In contrast, Cloudman S91 exosomes promoted T cell proliferation and Melan-A exosomes had a negligible effect on primary CD8+ T cells. Collectively, the results are consistent with somatic editing of exosomal payloads and suggest that exosomes establish a density-dependent field effect by altering the activity of immune cells that enter the tumor microenvironment.
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Project description:We recently showed that exosomes from primary AML cells and cell lines have potent regulatory capacity and we hypothesized that leukemia cell exosome trafficking might account for the suppression of residual hematopoietic stem and progenitor cells (HSPC) in the leukemic niche. Here we studied Molm-14 cells in in vitro experiments using purified exosomes under carefully calibrated low-oxygen conditions. This approach revealed the active regulation of stromal- and hematopoietic progenitor cell function. Systematic analysis of AML exosomes identified a panel of differentially enriched hypoxia-responsive miRNAs, including miR-210, -155, and -146a. We cultured cells under normoxic and hypoxic conditions. Exosomes were released from the parental cells and captured. Total RNA was isolated from both exosomes and cells. Please note that the sample numbers (in the titles) do differ from pair identification (i.e. pair ID) as the pair is only in reference to the paired-t test and parental vs. released pairs.
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