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accession-icon GSE68837
Expression data from cell lines forced expressed PGC7/Stella
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Global DNA hypomethylation and DNA hypermethylation of promoter regionsincluding tumor suppressor genesare frequently detected in human cancers. Although many studies have suggested a contribution to carcinogenesis, it is still unclear whether the aberrant DNA hypomethylation observed in tumors is a consequence or a cause of cancer. We found that overexpression of Stella (also known as PGC7, Dppa3), a maternal factor required for the maintenance of DNA methylation in early embryos, induced global DNA hypomethylation and transformation in NIH3T3 cells. This hypomethylation was due to the binding of Stella to Np95 (also known as Uhrf1, ICBP90) and the subsequent impairment of Dnmt1 localization. In addition, enforced expression of Stella enhanced the metastatic ability of B16 melanoma cells through the induction of metastasis-related genes by inducing DNA hypomethylation of their promoter regions. Such DNA hypomethylation itself causes cellular transformation and metastatic ability. These data provide new insight into the function of global DNA hypomethylation in carcinogenesis.

Publication Title

Global DNA hypomethylation coupled to cellular transformation and metastatic ability.

Sample Metadata Fields

Cell line

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accession-icon GSE90922
Expression data in JDCaP prostate cancer xenograft model before and after expression of AR splice variants
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Our previous study using nude rats revealed that the parental JDCaP xenografts predominantly expressed full-length androgen receptor (AR) whereas the relapsed JDCaP xenografts after castration acquired AR splice variants including AR-V7 and ARv567es. To understand molecular mechanisms underlying the acquisition of AR splice variants in the JDCaP model, we performed microarray analysis using RNA samples of the xenografts without castration (Parent), the relapsed xenografts overexpressing full-length AR and AR-V7 (ARhiV7hi), and the relapsed xenografts expressing ARv567es (ARv567es).

Publication Title

The RNA helicase DDX39B and its paralog DDX39A regulate androgen receptor splice variant AR-V7 generation.

Sample Metadata Fields

Specimen part

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accession-icon GSE36360
The effect of over-expression of PRR5-VP in Arabidopsis seedlings
  • organism-icon Arabidopsis thaliana
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

PRR5 transcription factor acts in the circadian clock system. To elucidate regulated genes by PRR5, Chimeric protein PRR5-VP, which activates direct target genes of PRR5, was over-expressed in Col-0. Microarray analsysis was performed using these plants with Affymetrix ATH1 genechip.

Publication Title

Transcriptional repressor PRR5 directly regulates clock-output pathways.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE66604
Inhibition of ABCB1 Overcomes Cancer Stem Cell-like Properties and Acquired Resistance to MET inhibitor in Non-Small Cell Lung Cancer
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Non-small cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) mutations have shown a dramatic response to EGFR inhibitors (EGFR-TKI). EGFR T790M mutation and MET amplification have been recognized as major mechanisms of acquired resistance to EGFR-TKI. Therefore, MET inhibitors have recently been used in NSCLC patients in clinical trials. In this study, we tried to identify the mechanism of acquired resistance to MET inhibitor. We analyzed the antitumor effects of two MET inhibitors, PHA-665752 and crizotinib, in 10 NSCLC cell lines. EBC1 cells with MET amplification were the only cells that were sensitive to both MET inhibitors. We established PHA-665752-resistant EBC1 cells, namely EBC1-R cells. EBC1-R cells showed overexpression of ATP-binding cassette sub-family B member 1 (ABCB1) as well as phosphorylation of MET. EBC1-R cells grew as cell spheres that exhibited cancer stem cell-like (CSC) properties and epithelial mesenchymal transition (EMT). The levels of two miRNAs, miR-374a and miR-138 which targeted ABCB1, were decreased in EBC1-R cells. ABCB1 siRNA and ABCB1 inhibitor elacridar could reduce sphere numbers and suppress EMT. Elacridar could also reverse the resistance to PHA-665752 in EBC1-R cells. Our study demonstrated that ABCB1 overexpression which was associated with CSC properties and EMT was involved in the acquired resistance to MET inhibitor. Inhibition of ABCB1 might be a novel therapeutic strategy for NSCLC patients with acquired resistance to MET inhibitor.

Publication Title

Inhibition of ABCB1 Overcomes Cancer Stem Cell-like Properties and Acquired Resistance to MET Inhibitors in Non-Small Cell Lung Cancer.

Sample Metadata Fields

Cell line

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accession-icon SRP032537
Transcriptome of Nkx2-5-null atria
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

Atrial specific knockout of Nkx2-5 results in hyperplastic atria with ASD and conduction defects. To examine how Nkx2-5 regulates cardiac proliferation at late gestational stages, RNA-seq was performed. Overall design: Examination of expression profile of 2 Nkx2-5-null atria and 3 controls

Publication Title

Nkx2-5 suppresses the proliferation of atrial myocytes and conduction system.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE28091
Expression profiles of mouse glioma-initiating cells.
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To identify factors involved in glioma-initiating cells (GICs), we compared gene expressions between GIC-like cells and non-GICs.

Publication Title

Combination of a ptgs2 inhibitor and an epidermal growth factor receptor-signaling inhibitor prevents tumorigenesis of oligodendrocyte lineage-derived glioma-initiating cells.

Sample Metadata Fields

Specimen part

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accession-icon GSE17062
Expression profiling of mouse glioma-initiating cell-like cells (GICs) and non-GICs
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To identify factors involved in glioma-initiating cells (GICs), we compared gene expression between GIC-like cells and non-GICs.

Publication Title

Sox11 prevents tumorigenesis of glioma-initiating cells by inducing neuronal differentiation.

Sample Metadata Fields

Specimen part

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accession-icon GSE17076
Expression profiling of sox11-expressing glioma-initiating cell-like cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To identify factors involved in tumorigenicity of glioma-initiating cells (GICs), we compared gene expression in GIC-like cells with and without sox11 expression.

Publication Title

Sox11 prevents tumorigenesis of glioma-initiating cells by inducing neuronal differentiation.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE14319
Genetic Control of Cellular Quiescence in S. pombe
  • organism-icon Schizosaccharomyces pombe
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Transition from proliferation to quiescence brings about extensive changes in cellular behavior and structure. However, genes critical for establishing and/or for maintaining quiescence are largely unknown. The fission yeast S. pombe is found as an excellent model for studying this problem, because it becomes quiescent under nitrogen starvation. Here we characterize 610 temperature-sensitive (ts) mutants, and identify 33 genes required for entry into and the maintenance of quiescence. These genes cover a broad range of cellular functions in the cytoplasm, membrane and the nucleus, encoding proteins for stress-responsive and cell cycle kinase signaling pathway, actin-bound and osmo-controlling endosome formation, RNA transcription, splicing and ribosome biogenesis, chromatin silencing, biosynthesis of lipid and ATP, cell wall and membrane morphogenesis, protein trafficking and vesicle fusion. We specifically highlight Fcp1, CTD phosphatase of RNA polymerase II, which differentially affects transcription of genes involved in quiescence and proliferation. We propose that the transcriptional role of Fcp1 is central to differentiate quiescence from proliferation.

Publication Title

Genetic control of cellular quiescence in S. pombe.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE19589
Effect of odorant inhalation on hypothlamic gene expression profile exposed to restraint stress in rats
  • organism-icon Rattus norvegicus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

As an attempt to assess physio-psychological effects elicited in odorant-inhaled rats, gene expression profiling in the central nervous system was carried out with rats housed under stressful conditions. (R)-(-)-linalool inhalation to rats during 2 h restraint significantly up-regulated the expression of genes in hypothalamus, which were found to be related to neuron differentiation and regulation of transcription as well as immediate early genes. The expressions of 104 among focused stress-regulated genes were significantly altered by the inhalation. The (R)-(-)-linalool inhalation significantly repressed the restraint-induced changes in the expression levels of 77 of the 104. It also promoted the expression of the remaining 27 genes including those related to anti-apoptotic heat shock proteins. The differences in their hypothalamic gene expressions revealed that the inhaled odorants actually influenced stress responses, based on the restraint-induced hypothalamic gene expressions related to apoptosis. These results indicate that the analysis of gene expression profiles in rats subjected to a stressful condition is useful to evaluate odorant-induced effects as shown by the particular results that (R)-(-)-linalool inhalation under only 2 h restraint- stressed condition induces neuron differentiation against apoptosis.

Publication Title

Neuron differentiation-related genes are up-regulated in the hypothalamus of odorant-inhaling rats subjected to acute restraint stress.

Sample Metadata Fields

Sex, Specimen part

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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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