Filters
Technology
Platform
GSE41678
Homo sapiens
79 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Weve undertaken a genome-wide approach to identify and test genes in fibroblasts that are both induced upon interaction with basal breast cancer cells in culture and upregulated in stromal cells from primary human breast cancers. Several of the upregulated genes encode secreted growth factors or cytokines. Using RNAi and a co-injection tumorigenicity assay, we determined that the majority of secreted factors selected for functional validation played significant, yet functionally diverse, roles in promoting tumorigenicity. Rather than a single major mediator, these results indicate multiple points of intervention to prevent fibroblasts from supporting basal breast cancer. Additionally, we show that breast cancer subtypes differ markedly in the expression of these and other stromally secreted proteins using data from microdissected stromal samples.
Publication Title
System-wide analysis reveals a complex network of tumor-fibroblast interactions involved in tumorigenicity.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 2 Downloadable Samples
Illumina Genome Analyzer
Description
Natural killer (NK) cells play a critical role in early host defense to infected and transformed cells. Here we show that mice deficient in Eri1, a conserved 3’-to-5’ exoribonuclease that represses RNA interference, have a cell-intrinsic defect in NK cell development and maturation. Eri1–/– NK cells displayed delayed acquisition of Ly49 receptors in the bone marrow and a selective reduction in Ly49D and Ly49H activating receptors in the periphery. Eri1 was required for immune-mediated control of mouse cytomegalovirus (MCMV) infection. Ly49H+ NK cells deficient in Eri1 failed to expand efficiently during MCMV infection, and virus-specific responses were also diminished among Eri1–/– T cells. We identified miRNAs as the major endogenous small RNA target of Eri1 in mouse lymphocytes. Both NK and T cells deficient in Eri1 displayed a global, sequence-independent increase in miRNA abundance. Ectopic Eri1 expression rescued defective miRNA expression in mature Eri1–/– T cells. Thus, mouse Eri1 regulates miRNA homeostasis in lymphocytes and is required for normal NK cell development and anti-viral immunity. Overall design: Small RNA profiling from wildtype and Eri1-deficient mouse CD4+ T cells
Publication Title
Eri1 regulates microRNA homeostasis and mouse lymphocyte development and antiviral function.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Saccharomyces cerevisiae
- 3 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
RPA12 is a subunit of RNA polymerase I.
Publication Title
Microarray data analyses of yeast RNA Pol I subunit RPA12 deletion strain.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 44 Downloadable Samples
- Illumina HiSeq 2500
Description
The synergistic regimen CT-VT-RT triggers proinflammatory antiviral signalling with activation of apoptotic cascades resulting in tumor cell death. Overall design: The experiment was designed to elicit individual treatment effects using monotherapies to understand the combinatorial sequential effect of dual and triple regimen using appropriate controls.
Publication Title
Measles Virus-Based Treatments Trigger a Pro-inflammatory Cascade and a Distinctive Immunopeptidome in Glioblastoma.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject, Time
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Estrogens and progesterone control mammary gland development and breast carcinogenesis via their cognate receptors expressed in a subset of cells of the luminal layer of the mammary epithelium. The extracellular matrix (ECM) including the basement membrane (BM) is important in breast physiology and tumorigenesis but how epithelial hormone receptor signaling and ECM are linked mechanistically is unclear. We identify the secreted protease Adamts18 as critical intermediary. Luminal estrogen and progesterone receptor signaling via upregulation of Wnt4 expression and ensuing canonical Wnt signaling activation in basal cells control Adamts18 expression there. The protease has an epithelial-intrinsic role in stem cell activation. We identify multiple binding partners in the interstitial ECM and BM and show that ADAMTS18 cleaves fibronectin in vitro. Its deletion results in increased fibronectin, collagen I and IV, and laminin deposition in pubertal glands. Adamts18 interacts genetically with Col18a1, which encodes a proteoglycan that is BM-specific, in stem cell regulation. Adamts18 inactivation impairs Hippo signaling and reduces Fgfr2 expression and signaling, which are vital for stem cell function. Our findings link epithelial hormone signaling to BM remodeling by Adamts18, and define the BM as an essential stem cell niche component.
Publication Title
The secreted protease Adamts18 links hormone action to activation of the mammary stem cell niche.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We hypothesized that gene expression in lungs of Fra-1+/+ and Fra-1-/- mice are divergent thus contributing fibrosis. More specifically, Fra-1-/- mice are increased susceptible to fibrosis. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between Fra-1+/+ and Fra-1-/- mice at early time point.
Publication Title
Expression profiling of genes regulated by Fra-1/AP-1 transcription factor during bleomycin-induced pulmonary fibrosis.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 22 Downloadable Samples
- Illumina HumanWG-6_V2_0_R2
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Tumour-initiating stem-like cells in human prostate cancer exhibit increased NF-κB signalling.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 22 Downloadable Samples
- Illumina HumanWG-6_V2_0_R2
Description
Human prostate CWR22 OT-tumor cells were prospectively purified for expression of various stem cell markers (TRA-1-60/CD151/CD166/EpCAM/CD44/2-Integrin). Unsorted total tumor cells or the additional marker positive cells that do not manifest stem-like characteristics were used as control. All these cells were subjected to molecular profiling of total RNA expression and the fold change data are tabulated according to S/TFE of the purified cells in relation to their control.
Publication Title
Tumour-initiating stem-like cells in human prostate cancer exhibit increased NF-κB signalling.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 1 Downloadable Sample
- Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
ABSTRACT Background: Viral myocarditis is a life-threatening illness that may lead to heart failure or cardiac arrhythmias. This study examined whether human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) could be used to model the pathogenic processes of coxsackievirus-induced viral myocarditis and to screen antiviral therapeutics for efficacy. Methods and Results: Human iPSC-CMs were infected with a luciferase-expressing mutant of the coxsackievirus B3 strain (CVB3-Luc). Brightfield microscopy, immunofluorescence, and calcium imaging were used to characterize virally infected hiPSC-CMs. Viral proliferation on hiPSC-CMs was subsequently quantified using bioluminescence imaging. For drug screening, select antiviral compounds including interferon beta 1 (IFN1), ribavirin, pyrrolidine dithiocarbamate (PDTC), and fluoxetine were tested for their capacity to abrogate CVB3-Luc proliferation in hiPSC-CMs in vitro. The ability of some of these compounds to reduce CVB3-Luc proliferation in hiPSC-CMs was consistent with the reported drug effects in previous studies. Finally, mechanistic analyses via gene expression profiling of hiPSC-CMs infected with CVB3-Luc revealed an activation of viral RNA and protein clearance pathways within these hiPSC-CMs after IFN1 treatment. Conclusions: This study demonstrates that hiPSC-CMs express the coxsackievirus and adenovirus receptor, are susceptible to coxsackievirus infection, and can be used to confirm antiviral drug efficacy. Our results suggest that the hiPSC-CM/CVB3-Luc assay is a sensitive platform that could be used to screen novel antiviral therapeutics for their effectiveness in a high-throughput fashion.
Publication Title
Human induced pluripotent stem cell-derived cardiomyocytes as an in vitro model for coxsackievirus B3-induced myocarditis and antiviral drug screening platform.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 42 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Objective: Conflicting evidence exists regarding the suppressive capacity of Tregs from the peripheral blood (PB) of patients with rheumatoid arthritis (RA). Our aim was to determine whether Tregs are intrinsically defective in RA using a wide range of read-out assays. Methods: CD3+CD4+CD25+CD127low Tregs from CD45RO+ and CD45RA+ compartments of PB from patients with RA and healthy controls (HC) were analysed for phenotype, cytokine expression profile (ex vivo and after in vitro stimulation), suppression of effector T-cell proliferation and cytokine production, suppression of monocyte-derived cytokine/chemokine production, and gene expression profiling. Results: No differences were observed between patients with RA and HC regarding Treg frequency, ex vivo phenotype (CD4, CD25, CD127, CD39, CD161) or pro-inflammatory cytokine profile (IL-17, IFN-gamma, TNF-alpha). FOXP3 expression was increased in Tregs from RA blood. The ability of Tregs to suppress T-cell proliferation or cytokine (IFN-gamma, TNF-alpha) production upon co-culture with autologous CD45RO+ effector T-cells and monocytes was not significantly different between patients with RA and HC. CD45RO+ Tregs from RA blood showed a slightly impaired ability to suppress production of some cytokines/chemokines by autologous LPS-activated monocytes (IL-1-beta, IL-1Ra, IL-7, CCL3, CCL4), but this was not true for all patients and other cytokines/chemokines (TNF-alpha, IL-6, IL-8, IL-12, IL-15, CCL5) were suppressed in the majority of patients similarly to HC. Finally, gene expression profiling of CD45RA+ or CD45RO+ Tregs from PB revealed no statistically significant differences between patients with RA and HC. Conclusions: Our findings suggest that Tregs isolated from PB of patients with RA are not intrinsically defective.
Publication Title
Phenotypic, Functional, and Gene Expression Profiling of Peripheral CD45RA+ and CD45RO+ CD4+CD25+CD127(low) Treg Cells in Patients With Chronic Rheumatoid Arthritis.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Subject
View Samples