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accession-icon GSE98265
Stress signaling in breast cancer cells induces matrix components that promote chemoresistant metastasis
  • organism-icon Homo sapiens
  • sample-icon 27 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

Stress signaling in breast cancer cells induces matrix components that promote chemoresistant metastasis.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE98237
Genes regulated by JNK signaling in MDA231-LM2 breast cancer cells
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In advanced malignancies, cancer cells have acquired capabilities to resist a variety of stress-inducing insults. We show that c-Jun N-terminal kinase (JNK) stress signaling is highly active in cancer cells from patients with late stage breast cancer and promotes tumor growth and metastasis in mouse models. Transcriptomic analysis revealed that JNK activity induces genes associated with extracellular matrix (ECM), wound healing and mammary stem cells. The ECM proteins and niche components osteopontin (SPP1) and tenascin C (TNC) are induced by JNK signaling and promote metastatic colonization of the lungs. Notably, treatment with chemotherapeutic drugs induces JNK activity in breast cancer cells, reinforcing the production of SPP1 and TNC. Inhibition of JNK or reduction of SPP1 or TNC expression sensitizes primary tumors and metastases in mice to chemotherapy.

Publication Title

Stress signaling in breast cancer cells induces matrix components that promote chemoresistant metastasis.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE98239
Gene expression data in MDA231-LM2 breast cancer cells cultured as oncospheres
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In advanced malignancies, cancer cells have acquired capabilities to resist a variety of stress-inducing insults. We show that c-Jun N-terminal kinase (JNK) stress signaling is highly active in cancer cells from patients with late stage breast cancer and promotes tumor growth and metastasis in mouse models. Transcriptomic analysis revealed that JNK activity induces genes associated with extracellular matrix (ECM), wound healing and mammary stem cells. The ECM proteins and niche components osteopontin (SPP1) and tenascin C (TNC) are induced by JNK signaling and promote metastatic colonization of the lungs. Notably, treatment with chemotherapeutic drugs induces JNK activity in breast cancer cells, reinforcing the production of SPP1 and TNC. Inhibition of JNK or reduction of SPP1 or TNC expression sensitizes primary tumors and metastases in mice to chemotherapy.

Publication Title

Stress signaling in breast cancer cells induces matrix components that promote chemoresistant metastasis.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE98238
Gene expression data in MDA231-LM2 breast cancer cells exposed to paclitaxel chemotherapy
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In advanced malignancies, cancer cells have acquired capabilities to resist a variety of stress-inducing insults. We show that c-Jun N-terminal kinase (JNK) stress signaling is highly active in cancer cells from patients with late stage breast cancer and promotes tumor growth and metastasis in mouse models. Transcriptomic analysis revealed that JNK activity induces genes associated with extracellular matrix (ECM), wound healing and mammary stem cells. The ECM proteins and niche components osteopontin (SPP1) and tenascin C (TNC) are induced by JNK signaling and promote metastatic colonization of the lungs. Notably, treatment with chemotherapeutic drugs induces JNK activity in breast cancer cells, reinforcing the production of SPP1 and TNC. Inhibition of JNK or reduction of SPP1 or TNC expression sensitizes primary tumors and metastases in mice to chemotherapy.

Publication Title

Stress signaling in breast cancer cells induces matrix components that promote chemoresistant metastasis.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE57118
Heterogeneous stock rats that differ in glucose tolerance
  • organism-icon Rattus norvegicus
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Identification of a novel gene for diabetic traits in rats, mice, and humans.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
accession-icon GSE54935
Gene expression profiles in heterogeneous stock rats that differ in glucose tolerance
  • organism-icon Rattus norvegicus
  • sample-icon 58 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Using heterogeneous stock (HS) rats, we have identified a region on rat chromosome 1 that maps multiple diabetic traits. We sought to use global expression analysis to determine if genes within this region are differentially expressed between HS rats with normal glucose tolerance and those with glucose intolerance

Publication Title

Identification of a novel gene for diabetic traits in rats, mice, and humans.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples
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

No sample metadata fields

View Samples
accession-icon GSE46390
Expression data from peritoneal macrophages
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Colony Stimulating Factor 1(CSF1) is known to promote osteoclast progenitor survival but its role in regulating osteoclast differentiation and mature osteoclast function are less well understood.

Publication Title

The transcription factor T-box 3 regulates colony-stimulating factor 1-dependent Jun dimerization protein 2 expression and plays an important role in osteoclastogenesis.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

View Samples
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

View Samples
accession-icon GSE67375
Neuropathic Gaucher mouse brain
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Neuronopathic Gaucher disease: dysregulated mRNAs and miRNAs in brain pathogenesis and effects of pharmacologic chaperone treatment in a mouse model.

Sample Metadata Fields

Specimen part

View Samples

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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