Ontology highlight
ABSTRACT:
PROVIDER: PRJNA478383 | ENA |
REPOSITORIES: ENA
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Project description:To investigate how gene expression profiles change in CD8+ T cells based on time, tumor burden, and tissue localization, we orthotopically implanted the mouse lung adenocarcinoma HKP1 cell line expressing luciferase into syngeneic C57BL/6 mice by tail vein injections. Tumor growth was monitored by bioluminescence imaging. A separate cohort of mice received no tumor implantation. At days 7, 17, and 24 post tumor implantation, mice were euthanized and CD8+ T cells sorted from tumor-bearing lungs and spleens, or matched naive lungs and spleens. We then performed gene expression profiling analysis using data obtained from RNA-seq of sorted cells, comparing across time, tumor burden, and tissue localization.
2023-10-19 | GSE218141 | GEO
Project description:To identify tumor-specific transcriptional changes following SX-682 treatment, we performed RNA sequencing on each of the MelanA, B16F0, and B16F10 cell lines.
2023-06-07 | GSE223288 | GEO
Project description:The cell line-derived xenografts and patient derived xenografts have limited use in cancer immunotherapy evaluation because an immune compromised host is required for xenotransplantation. Syngeneic mouse models are derived by transplanting established mouse cell lines or tumor tissues to strain matched mouse hosts, which are better suited to study the interplay between immune and tumor cells. We investigated the differences as well as similarities of a panel of ten mouse syngeneic models to features of human tumors by proteomics, which will provide valuable information to assist experimental biologists in model selection.
2019-12-03 | PXD011885 | Pride
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.
2017-07-31 | GSE71610 | GEO
Project description:DHX15 is an ATP-dependent RNA helicase involved in pre-mRNA splicing. We have recently reported that DHX15 is a downstream substrate for Akt1, which plays a significant role in vascular biology. Therefore, we aimed to explore the regulatory function of DHX15 over the vasculature, and the endothelial cell biology in different contexts: development, metabolism, ischemia and tumor growth. Methods: Deficient DHX15 mice and zebrafish were generated using transcription activator-like effector nuclease (TALEN) and Crispr/cas9 gene edition. Lymphatic functionality was evaluated by lymphangiography and magnetic resonance imaging. Mouse-induced tumor and metastasis model were generated by injection of syngeneic LLC1 tumor cells. DHX15 gene silencing in mouse liver endothelial cells (LEC) was performed by the lentiviral transduction of shRNA (Dharmacon). The changes in the transcriptome and the proteome resulting from the shRNA transduction were investigated by RNAseq and mass spectrometry, respectively. Results: Homozygous DHX15 gene deficiency was lethal in mouse and zebrafish embryos. DHX15-/- zebrafish also showed an undeveloped parachordal line, which leads to the formation of lymphatic structures in the trunk during the development. DHX15+/- mice and zebrafish were viable, although DHX15+/- gene deficiency triggered lower vascular network density and impaired lymphatic function postnatally in mice. Whole transcriptome and proteome analysis of DHX15 silenced LEC revealed differential expression of enzymes involved in the glycolysis and the gluconeogenesis pathways. The functional validation of these results demonstrated an uncoupling of the glycolysis with the oxidation of pyruvate into the mitochondria and lower activity of the Complex I in the mitochondrial membrane, resulting in lower cellular ATP production. Noteworthy, heterozygous DHX15 deficiency partially inhibited primary tumor growth and reduced lung metastasis after injection of syngeneic LLC1 tumor cells, compared to wild-type mice
2021-11-04 | PXD018104 | Pride