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SRP166099
Mus musculus
4 Downloadable Samples
Illumina HiSeq 2500
Description
miR-155 has recently emerged as an important promoter of antitumor immunity through its functions in T lymphocytes. However, the impact of T cell expressed miR-155 on immune cell dynamics in solid tumors remains unclear. In the present study, we used single-cell RNA-sequencing to define the CD45+ immune cell populations within B16F10 murine melanoma tumors growing in either wild-type (WT) or miR-155 T cell conditional knockout (TCKO) mice at different timepoints. miR-155 was required for optimal T cell activation and reinforced the T cell response at the expense of infiltrating myeloid cells. Further, myeloid cells from tumors growing in TCKO mice were defined by an increase in wound healing genes and a decreased IFNg response gene signature. Finally, we found that miR-155 expression predicted a favorable outcome in human melanoma patients and was associated with a strong immune signature. Moreover, gene expression and histological analysis of the Cancer Genome Atlas (TCGA) data revealed that miR-155 expression also correlates with an immune-enriched subtype in 29 other human solid tumor types. Together, our study provides an unprecedented analysis of the cell types and gene expression signatures by immune cells within experimental melanoma tumors and elucidates miR-155's role in coordinating this dynamic response. Overall design: B16F10 murine melanoma cells expressing ovalbumin model antigen were injected subcutaneously (1e6) into wild-type (C57BL/6) and miR-155 T cell conditional knockout mice (n>4). 9 or 12 days after injection, tumors were pooled in each group, and DAPI(-)CD45(+) live tumor infiltrating immune cells were sorted via flow cytometry. Sorted immune cells were processed for single-cell RNA-sequencing via 10x platform.
Publication Title
MicroRNA-155 coordinates the immunological landscape within murine melanoma and correlates with immunity in human cancers.
Sample Metadata Fields
Specimen part, Cell line, Subject, Time
View Samples- Homo sapiens
- 18 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
It is known that natural killer (NK) cells are a heterogeneous population of functionally distinct NK cell subsets. Here we report on different genomic, phenotypic and functional properties of human NK cell subsets derived from peripheral blood, thymus and bone marrow. NK cell subpopulations were defined via expression of CD56 and CD16.
Publication Title
Specific phenotype and function of CD56-expressing innate immune cell subsets in human thymus.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Inflammatory Bowel Diseases are associated with marked alterations of IECs with a subsequent loss of barrier function.
Publication Title
Rho-A prenylation and signaling link epithelial homeostasis to intestinal inflammation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Prenylation is a post-translational modification of proteins consisting on the attachment of a lipid residue (isoprenoid). GGTase-I is one of the prenyltransferases catalyzing prenylation.
Publication Title
Rho-A prenylation and signaling link epithelial homeostasis to intestinal inflammation.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 9 Downloadable Samples
- Illumina HiSeq 2500
Description
Cancer cells alter their metabolism to support their malignant properties. By transcriptomic analysis we identified the glucose-transforming polyol pathway (PP) gene aldo-keto-reductase-1-member-B1 (AKR1B1) as strongly correlated with epithelial-to-mesenchymal transition (EMT). This association was confirmed staining samples from lung cancer patients and from an EMT-driven colon cancer mouse model with p53 deletion. In vitro, mesenchymal-like cancer cells showed increased AKR1B1 levels and AKR1B1 knockdown was sufficient to revert EMT. An equivalent level of EMT suppression was measured by targeting the downstream enzyme sorbitol-dehydrogenase (SORD), further pointing at the involvement of the PP. Comparative RNA sequencing profiling confirmed a profound alteration of EMT in PP-deficient cells, revealing a strong repression of TGF-Beta signature genes. Mechanistically, excess glucose was found to promote EMT through autocrine TGF-Beta stimulation, while PP-deficient cells were refractory to glucose-induced EMT. PP represents a molecular link between glucose metabolism and cancer differentiation and aggressiveness, and a novel potential therapeutic target. Overall design: 3x3 biological replicated samples; 2 groups of samples with shRNA-mediated specific gene inhibition and scrambled control cells
Publication Title
Polyol Pathway Links Glucose Metabolism to the Aggressiveness of Cancer Cells.
Sample Metadata Fields
Cell line, Treatment, Subject
View Samples