Filters
Technology
Platform
SRP174055
Homo sapiens
14 Downloadable Samples
Illumina HiSeq 2500
Description
Lung adenocarcinoma (LUAD)-derived oncogenic Wnts increase cancer cell proliferative/stemness potential, but whether they also impact the immune microenvironment is unknown. Here we show that LUAD cells use paracrine Wnt1 signaling to induce immune resistance. Wnt1 correlated strongly with tolerogenic genes on the TCGA expression data. In another cohort, Wnt1 was inversely associated with T cell abundance. Altering Wnt1 expression profoundly affected growth of murine lung adenocarcinomas and this was strongly dependent on conventional dendritic cells and T cells. Mechanistically, Wnt1 lead to transcriptional silencing of CC/CXC chemokines in dendritic cells and T cell cross-tolerance. Wnt-target genes were up-regulated in human intratumoral dendritic cells and decreased upon silencing Wnt1, accompanied by enhanced T cell cytotoxicity. siWnt1-loaded nanoparticles as single therapy or part of combinatorial immunotherapies acted at both arms of the cancer-immune ecosystem to halt tumor growth. Collectively, our studies show that Wnt1 enhances adaptive immune rejection of lung adenocarcinomas and highlight its potential targeting as a novel therapeutic strategy Overall design: RNAseq data of two DC subsets of 4 patients with lung adenocarcinomas (LUADs).
Publication Title
Wnt1 silences chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma.
Sample Metadata Fields
Sex, Age, Specimen part, Subject
View Samples- Mus musculus
- 5 Downloadable Samples
- Ion Torrent Proton
Description
This study showed that the oncogenic ligand Wnt1 silences chemokine genes in dendritic cells, leading to impaired cross-priming of T cells in lung adenocarcinoma. Blocking Wnt1 enhanced rejection of tumors by acting concomitantly at the cancer and immune cell level. Overall design: 3' RNA-Seq (QuantSeq) profiling of sorted cDCs populations from WNT1 overexpressing and control (Empty) lung tumors.
Publication Title
Wnt1 silences chemokine genes in dendritic cells and induces adaptive immune resistance in lung adenocarcinoma.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
We compared different mouse cancer cell lines to identify their unique cell signatures.
Publication Title
<i>NRAS</i> destines tumor cells to the lungs.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Both environmental and genetic factors play important roles in the development of the metabolic syndrome. To elucidate how these factors interact under normal conditions, C57Bl/6 (B6) and 129S6/SvEvTac (129) mice were placed on a low-fat or high-fat diet. Liver samples were extracted and hybridized to Affymetrix Genome U74 (version 2) arrays.
Publication Title
Effects of diet and genetic background on sterol regulatory element-binding protein-1c, stearoyl-CoA desaturase 1, and the development of the metabolic syndrome.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Murine Genome U74A Array (mgu74a)
Description
Loss of stearoyl-CoA desaturase-1 function protects mice against adiposity.
Publication Title
Loss of stearoyl-CoA desaturase-1 function protects mice against adiposity.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 18 Downloadable Samples
- Ion Torrent Proton
Description
This study demonstrates that arthritis and heart valve stenosis comorbidity, the most common condition among RA and SpA patients, share common mesenchymal requirements converging in the pathogenic activation of resident mesenchymal origin fibroblasts in the Tnf?ARE mouse model. TNFR2 signaling, in this context, orchestrates the molecular mechanisms underlying arthritis and heart valve stenosis manifestation by regulating fibroblasts pathogenic activation status, cell proliferation and pro-inflammatory milieu. Finally this work highlights the complexity of TNFR2 functions since mesenchymal signaling is detrimental, whereas systemic TNFR2 provides protective signals that contain both pathologies Overall design: 3' RNA-Seq (QuantSeq) profiling of 2 cell types (SFs,VICs) in two different genotypes (TNF-DeltaARE, ColVIp75f/f-TNF-DeltaARE) and Wild type as control. 3 replicates per group.
Publication Title
Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 20 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Stearoyl-CoA desaturase 1-deficient (SCD1-/-) mice have impaired monounsaturated fatty acid (MUFA) synthesis. When maintained on a very low-fat, high-carbohydrate (VLF-HC) diet, SCD1-/- mice develop severe hypercholesterolemia characterized by an increase in apolipoprotein B-containing lipoproteins and the appearance of lipoprotein-X. Additionally, high-density lipoprotein cholesterol is dramatically reduced in VLF-HC SCD1-/- mice. The concomitant presence of elevated plasma bile acids, bilirubin and aminotransferases in the VLF-HC SCD1-/- mouse are indicative of hepatic dysfunction. Supplementation of the VLF-HC diet with unsaturated fat (canola oil), but not saturated fat (coconut oil), prevents these plasma phenotypes. However, dietary oleate was not as effective as canola oil in reducing low-density lipoprotein cholesterol, signifying an additional role for dietary polyunsaturated fatty acid deficiency in the development of this phenotype. These results indicate that lack of SCD1 results in an increased requirement for dietary unsaturated fat to compensate for impaired MUFA synthesis and to prevent hypercholesterolemia and hepatic dysfunction.
Publication Title
Cholestasis and hypercholesterolemia in SCD1-deficient mice fed a low-fat, high-carbohydrate diet.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
N-octanoyl dopamine (NOD), but not dopamine dose dependently induces the UPR. This was also found for other synthetic N-Acyl dopamine derivates (NADD). Induction of the UPR was dependent on the redox activity of NADD and was not caused by selective activation of a particular UPR sensor. UPR induction did not result in cell apoptosis, yet NOD strongly impaired cell proliferation by attenuation of cells in the S-G2/M phase. Long-term treatment of HUVEC with low NOD concentration showed decreased intracellular ATP concentration paralleled with activation of AMPK. These cells were significantly more resistant to cold inflicted injury.
Publication Title
N-octanoyl dopamine treatment of endothelial cells induces the unfolded protein response and results in hypometabolism and tolerance to hypothermia.
Sample Metadata Fields
Cell line, Treatment
View Samples