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accession-icon SRP148097
Quiescent glioblastoma cells shift to an epithelial-mesenchymal transition-like gene program
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Quiescent stem cells of glioblastoma (GBM), a malignant primary brain tumor, are potential sources for recurrence after therapy. However, the gene expression program underlying the physiology of GBM stem cells remains unclear. We have isolated quiescent GBM cells by engineering them with a knock-in H2B-GFP proliferation reporter and expanding them in a 3D tumor organoid model that mimics tumor heterogeneity. H2B-GFP label retaining quiescent cells were subjected to stem cell assays and RNA-Seq gene expression analysis. While quiescent GBM cells were similar in clonal culture assays to their proliferative counterparts, they displayed higher therapy resistance. Interestingly, quiescent GBM cells upregulated epithelial-mesenchymal transition (EMT) genes and genes of extracellular matrix components. Our findings connect quiescent GBM cells with an EMT-like shift, possibly explaining how GBM stem cells achieve high therapy resistance and invasiveness, and suggest new targets to abrogate GBM. Overall design: Glioblastoma cancer cells in 3D organoid culture were pulsed for 2 weeks with H2B-GFP, then chased either 2 or 4 weeks. Label-retaining GFP-high cells (quiescent) were separated from bulk population, and both populations were analyzed by RNA-Seq.

Publication Title

Gene signatures of quiescent glioblastoma cells reveal mesenchymal shift and interactions with niche microenvironment.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP063867
Comparing isogenic pairs of hESC and hiPSC lines reveals genetic background and reprogramming method as primary sources of transcriptional variation
  • organism-icon Homo sapiens
  • sample-icon 73 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

The equivalency of human induced pluripotent stem cells (hiPSCs) with human embryonic stem cells (hESCs) remains controversial. Here, we devised a strategy to assess the contribution of clonal growth, reprogramming method and genetic background to transcriptional patterns in hESCs and hiPSCs. Surprisingly, transcriptional variation originating from two different genetic backgrounds was dominant over variation due to the reprogramming method or cell type of origin of pluripotent cell lines. Moreover, the few differences we detected between isogenic hESCs and hiPSCs neither predicted functional outcome, nor distinguished an independently derived, larger set of unmatched hESC/hiPSC lines. We conclude that hESCs and hiPSCs are transcriptionally and functionally highly similar and cannot be distinguished by a consistent gene expression signature. Our data further imply that genetic background variation is a major confounding factor for transcriptional comparisons of pluripotent cell lines, explaining some of the previously observed expression differences between unmatched hESCs and hiPSCs. Overall design: Expression profiling of human embryonic stem cells (ESCs), induced pluripotent stem cells (iPSCs) and fibroblasts, mostly in triplicates.

Publication Title

A comparison of genetically matched cell lines reveals the equivalence of human iPSCs and ESCs.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP134015
Single-cell transcriptome dynamics in stabilized pituitary gonadotrope cells [mini_dropseq]
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Studying dynamic transcripts in single cells (SC) requires large numbers of timed samples. We report an easy to use protocol to stabilize RNA in intact SCs without perturbing transcriptional patterns, and demonstrate its applicability for SC transcriptome assays with cells and tissue. We identify a gene-specific hierarchical pattern of all-or-none transcript induction elicited by different concentrations of pulsatile hormone stimuli in pituitary gonadotropes. Overall design: SC Mini Drop-seq experiments were performed on two samples from dissociated human cortical tissue: one is neocortex from a glioblastoma multiforme (GBM, tumor), the other is normal neocortex adjacent to the tumor.

Publication Title

Single-cell stabilization method identifies gonadotrope transcriptional dynamics and pituitary cell type heterogeneity.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE46498
Atrial Identity Is Determined by A COUP-TFII Regulatory Network
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Atrial identity is determined by a COUP-TFII regulatory network.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE46496
Atrial Identity Is Determined by A COUP-TFII Regulatory Network (RNA)
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Atria and ventricles exhibit distinct molecular profiles that produce structural and functional differences between the two cardiac compartments. However, factors that determine these differences remain largely undefined. Cardiomyocyte-specific COUP- TFII ablation produces ventricularized atria that exhibit ventricle-like action potentials, increased cardiomyocyte size, and development of extensive T-tubules.

Publication Title

Atrial identity is determined by a COUP-TFII regulatory network.

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP124503
A revised airway epithelial hierarchy includes CFTR-expressing ionocytes
  • organism-icon Mus musculus
  • sample-icon 325 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Airways conduct gases to the lung and are disease sites of asthma and cystic fibrosis. Here we study the cellular composition and hierarchy of the mouse tracheal epithelium by single-cell RNA-sequencing (scRNA-seq) and in vivo lineage tracing. We identify a rare cell type, the Foxi1+ pulmonary ionocyte; functional variations in club cells by proximodistal location; a distinct cell type in high turnover squamous epithelial structures that we term ''hillocks''; and disease-relevant subsets of tuft and goblet cells. We developed ''pulse-seq'' , combining scRNA-seq and lineage tracing, to show that tuft, neuroendocrine and ionocyte cells are continually and directly replenished by basal progenitor cells. Ionocytes are the major source of transcripts of the cystic fibrosis transmembrane conductance regulator in both mouse (Cftr) and human (CFTR). Knockout of Foxi1 in mouse ionocytes causes loss of Cftr expression and disrupts airway fluid and mucus physiology, phenotypes that characterize cystic fibrosis. By associating cell-type-specific expression programs with key disease genes, we establish a new cellular narrative for airways disease. Overall design: To understand normal tissue homeostasis, untreated cells were profiled using both 3''-droplet-based and full length plate-based single-cell RNAseq, in combination with genetic reporter-based lineage tracing.

Publication Title

A revised airway epithelial hierarchy includes CFTR-expressing ionocytes.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject, Time

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accession-icon GSE33182
Expression data from control and COUP-TFII siRNA treated PC3 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

COUP-TFII, a member of the nuclear receptor superfamily plays a critical role in angiogenesis and organogenesis during embryonic development. Our results indicate that COUP-TFII expression is profoundly upregulated in prostate cancer patients and might serves as biomarker for recurrence prediction. Thus we conduct transcriptome comparison of control and COUP-TFII depleted PC3 cells to gain genomic insights on the biological processes that COUP-TFII is involved in prostate cancer cells. Ingenuity Pathway Analysis (IPA) shows that the most prominent altered pathways in the COUP-TFII depleted cells are related to cell growth; cell cycle progression and DNA damage response. Indeed many growth related genes including E2F1, p21, CDC25A, Cyclin A and Cyclin B are changed in COUP-TFII knockdown cells, suggesting that COUP-TFII might be an important regulator for prostate cancer cell growth. Further functional assays from cells and mice genetic studies confirm the hypothesis that COUP-TFII serve as the major regulator to control prostrate cancer growth. Together, results provide insight into the role of COUP-TFII in prostate tumorigenesis.

Publication Title

COUP-TFII inhibits TGF-β-induced growth barrier to promote prostate tumorigenesis.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE37046
Combined microRNA/mRNA transcriptome analysis reveals angiogenic microRNAs-genes pathway of human late endothelial precursor cells.
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Deficiency of the microRNA-31-microRNA-720 pathway in the plasma and endothelial progenitor cells from patients with coronary artery disease.

Sample Metadata Fields

Specimen part, Treatment, Time

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accession-icon GSE37045
Gene expression patterns of distinct human endothelial precursor cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Early EPCs (eEPCs) appear at less than 1 week in culture dishes, whereas late EPCs (LEPCs) appear late at 2-4 weeks. Distinct angiogenic properties between these two EPC subpopulations have been disclosed by the angiogenesis assay: late EPCs, but not eEPCs, form vascular networks de novo and are able to incorporate into vascular networks. On the contrary, eEPCs, but not late ones, indirectly augment tubulogenesis even when physically separated by a Transwell membrane, implying the involvement of a cytokine-based paracrine mechanism.

Publication Title

Deficiency of the microRNA-31-microRNA-720 pathway in the plasma and endothelial progenitor cells from patients with coronary artery disease.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon GSE37044
mRNA expression profiles in far-infrared treated human endothelial precursor cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

High glucose impairs the angiogenic activities of late endothelial precursor cells (EPC). We found that far infrared (FIR) treatment restored partially the activity of late EPC. However, the mechanisms are unclear. We performed gene expression microarray analysis to assess the expression profiles of high glucose-treated late EPC with or without FIR treatment.

Publication Title

Deficiency of the microRNA-31-microRNA-720 pathway in the plasma and endothelial progenitor cells from patients with coronary artery disease.

Sample Metadata Fields

Specimen part, Treatment

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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