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accession-icon SRP064434
Homo sapiens strain:iPSC of Hep G2 Transcriptome or Gene expression
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

compare the RNA-seq profile with the original

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP064477
Homo sapiens strain:hep G2 Transcriptome or Gene expression
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

RNS-seq

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP064541
Homo sapiens Transcriptome or Gene expression
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

The induced pluripotent stem-like cells from human gastric cell line, KMU-CS12 (CS12) were derived from putative human gastric stem cell/progenitor cell clone. CS12 expressed cancer cell phenotypes, i.e. the ability of anchorage-independent growth high frequency (44%) and to the expression of Oct4, a stemness marker and many types of cancer cells, and tumor development in immune deficient mice.

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP064548
Homo sapiens Transcriptome or Gene expression
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge IconIlluminaGenomeAnalyzerIIx

Description

ips CSN; KMU-CSN (CSN) is an immortal cell line that was derived from putative human gastricstem cell/progenitor cell clone, KMU-GI2

Publication Title

No associated publication

Sample Metadata Fields

No sample metadata fields

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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 GSE46542
Focal amplification of HOXD-harboring chromosome region is implicated in multiple-walled carbon nanotubes-induced carcinogenicity
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Amplificaition of HOXD9 and HOXD13 genes was found in MWCNTs induced carcinogencity. By overexpression or silence of of HOXD9 and HOXD13 gene may alter tumorigenicity.

Publication Title

No associated publication

Sample Metadata Fields

Cell line

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accession-icon GSE9727
Gene Expression in S49 Deathless (D-) cell variant
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

The second messenger cAMP acts via protein kinase A (PKA) to induce apoptosis by mechanisms that are poorly understood. Here, we assessed a role for mitochondria and analyzed gene expression in cAMP/PKA-promoted apoptosis by comparing wild-type (WT) S49 lymphoma cells and the S49 variant, D- (cAMP-deathless), which lacks cAMP-promoted apoptosis but has wild-type levels of PKA activity and cAMP-promoted G1 growth arrest. Treatment of WT, but not D-, S49 cells with 8-CPT-cAMP for 24 h induced loss of mitochondrial membrane potential, mitochondrial release of cytochrome c and Smac and increase in caspase-3 activity. Gene expression analysis (using Affymetrix 430 2.0 Arrays) revealed that WT and D- cells incubated with 8-CPT-cAMP have similar, but non-identical, extents of cAMP-regulated gene expression at 2h (~800 transcripts) and 6h (~1000 transcripts) (|Fold|>2, P<0.06); by contrast, at 24h ~2500 and ~1100 transcripts were changed in WT and D- cells, respectively. Using an approach that combined regression analysis, clustering and functional annotation to identify transcripts that showed differential expression between WT and D- cells, we found differences in cAMP-mediated regulation of mRNAs involved in transcriptional repression, apoptosis, the cell cycle, RNA splicing, Golgi and lysosomes. The 2 cell lines differed in CREB phosphorylation and expression of the transcriptional inhibitor Icer and in cAMP-regulated expression of genes in the Inhibitor of apoptosis (IAP) and Bcl families. The findings indicate that cAMP/PKA-promoted apoptosis of lymphoid cells occurs via mitochondrial-mediated events and imply that such apoptosis involves gene networks in multiple biochemical pathways.

Publication Title

Gene expression signatures of cAMP/protein kinase A (PKA)-promoted, mitochondrial-dependent apoptosis. Comparative analysis of wild-type and cAMP-deathless S49 lymphoma cells.

Sample Metadata Fields

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accession-icon GSE2413
Timecourse of Gene Expression responses to cAMP in S49 Cells
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Abstract

Publication Title

Gene expression patterns define key transcriptional events in cell-cycle regulation by cAMP and protein kinase A.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE24266
Yeast (Saccharomyces cerevisiae) Overexpression suppression study
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

To address the mechanisms of suppression, we analyzed time course of mRNA expression of four suppressed smc2-8 mutant strains.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE94589
Gene Expression In Drosophila Hearts Harboring Ion Channel Mutations
  • organism-icon Drosophila melanogaster
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Age-dependent electrical and morphological remodeling of the Drosophila heart caused by hERG/seizure mutations

Publication Title

Age-dependent electrical and morphological remodeling of the Drosophila heart caused by hERG/seizure mutations.

Sample Metadata Fields

No sample metadata fields

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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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