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accession-icon GSE50518
Shp2 Signaling Suppresses Senescence in PyMT-induced Mammary Gland Cancer in Mice
  • organism-icon Mus musculus
  • sample-icon 24 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

Shp2 signaling suppresses senescence in PyMT-induced mammary gland cancer in mice.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE50517
Shp2 Signaling Suppresses Senescence in PyMT-induced Mammary Gland Cancer in Mice [Mouse430_2 array]
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In this study, we have used techniques from cell biology, biochemistry, and genetics to investigate the role of the tyrosine phosphatase Shp2 in tumor cells of MMTV-PyMT mouse mammary glands. Genetic ablation or pharmacological inhibition of Shp2 induces senescence, as determined by the activation of senescence-associated -gal (SA--gal), cyclin-dependent kinase inhibitor 1B (p27), p53, and histone 3 trimethylated lysine 9 (H3K9me3). Senescence induction leads to inhibition of self-renewal of tumor cells and blockage of tumor formation and growth. A signaling cascade was identified that acts downstream of Shp2 to counter senescence: Src, Focal adhesion kinase and Map kinase inhibit senescence by activating the expression of S-phase kinase-associated protein 2 (Skp2), Aurora kinase A (Aurka), and the Notch ligand Delta-like 1 (Dll1), which block p27 and p53. Remarkably, the expression of Shp2 and of selected target genes predicts human breast cancer outcome. We conclude that therapies which rely on senescence induction by inhibiting Shp2 or controlling its target gene products may be useful in blocking breast cancer.

Publication Title

Shp2 signaling suppresses senescence in PyMT-induced mammary gland cancer in mice.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE50516
Shp2 Signaling Suppresses Senescence in PyMT-induced Mammary Gland Cancer in Mice [Mouse430A_2 array]
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

In this study, we have used techniques from cell biology, biochemistry, and genetics to investigate the role of the tyrosine phosphatase Shp2 in tumor cells of MMTV-PyMT mouse mammary glands. Genetic ablation or pharmacological inhibition of Shp2 induces senescence, as determined by the activation of senescence-associated -gal (SA--gal), cyclin-dependent kinase inhibitor 1B (p27), p53, and histone 3 trimethylated lysine 9 (H3K9me3). Senescence induction leads to inhibition of self-renewal of tumor cells and blockage of tumor formation and growth. A signaling cascade was identified that acts downstream of Shp2 to counter senescence: Src, Focal adhesion kinase and Map kinase inhibit senescence by activating the expression of S-phase kinase-associated protein 2 (Skp2), Aurora kinase A (Aurka), and the Notch ligand Delta-like 1 (Dll1), which block p27 and p53. Remarkably, the expression of Shp2 and of selected target genes predicts human breast cancer outcome. We conclude that therapies which rely on senescence induction by inhibiting Shp2 or controlling its target gene products may be useful in blocking breast cancer.

Publication Title

Shp2 signaling suppresses senescence in PyMT-induced mammary gland cancer in mice.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE107384
Genome-wide analysis of P8 sciatic nerve gene expression of control, Maf mutant and ErbB2 mutant mice
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Analysis of genes regulated by Maf and donwstream of ErbB2 in P8 Schwann cells

Publication Title

Maf links Neuregulin1 signaling to cholesterol synthesis in myelinating Schwann cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE54044
Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic -cell function (Expression data from islets of control and Insm1 conditional deleted adult pancreatic islets)
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The zinc finger factor Insm1 is known to regulate differentiation of pancreatic cells during development, Here we show that Insm1 is essential for the maintenance of functionally mature pancreatic cells in mice.

Publication Title

Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE35899
Expression data from Mammospheres
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The combined activation of Wnt/-catenin and MET/HGF is required for mammary cancer stem cell (MaCSC) maintenance. We generated mammospheres derived from tumors of mice harboring Wnt/Met signaling mutations on which we performed microarray analysis to evaluate gene expression signatures controlled by Wnt and MET pathways. We used the gene expression profiles to dissect the role and the functions of these pathways in MaCSCs.

Publication Title

Combined Wnt/β-catenin, Met, and CXCL12/CXCR4 signals characterize basal breast cancer and predict disease outcome.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon SRP173598
A C/EBPa–Wnt connection in gut homeostasis and carcinogenesis
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We explored the connection between C/EBPa (CCAAT/enhancer binding protein a) and Wnt signaling in gut homeostasis and carcinogenesis. C/EBPa was expressed in human and murine intestinal epithelia in the transit amplifying region of the crypts and was absent in intestinal stem cells and Paneth cells with activated Wnt signaling. In human colorectal cancer and murine APCMin/+ polyps, C/EBPa was absent from nuclear ß-catenin–positive tumor cells. In chemically induced intestinal carcinogenesis, C/EBPa KO in murine gut epithelia increased tumor volume. C/EBPa deletion extended the S-phase cell zone in intestinal organoids and activated typical proliferation gene expression signatures, including that of Wnt target genes. Genetic activation of ß-catenin in organoids attenuated C/EBPa expression. Comparing gene expression of wild type and C/EBPa KO organoids by RNA sequencing aimed to identify C/EBPa dependent alterations in gene expression. Overall design: These data suggest homeostatic and oncogenic suppressor functions of C/EBPa in the gut by restricting Wnt signaling.

Publication Title

A C/EBPα-Wnt connection in gut homeostasis and carcinogenesis.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP150258
Gene expression profiling of prostate basal cells at proximal and distal ducts
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

We have noticed that the proliferative potential of epithelial cells in the mouse proximal prostatic ducts is less than those at the distal prostatic ducts. To determine whether specific signaling is differentially activated in distal and proximal prostate basal cells, we isolated respective basal cells in the two regions and performed an RNA-seq analysis. Overall design: Two group comparison

Publication Title

Spatially Restricted Stromal Wnt Signaling Restrains Prostate Epithelial Progenitor Growth through Direct and Indirect Mechanisms.

Sample Metadata Fields

Specimen part, Cell line, Subject

View Samples
accession-icon SRP149995
Gene expression profiling of mouse prostate stromal cells with beta-catenin S37A mutation
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

To identify such inhibitory signaling mediated by the stromal cells with active Wnt activity, we performed an RNA-seq analysis comparing the gene expression profiles of primarily cultured adult mouse prostate stromal cells that express S37A ß-Catenin and the control cells that only express GFP. We identified 783 genes that were differentially expressed by at least 1.2 fold (Fig. 4A). Genes associated with the Wnt receptor signaling pathway were enriched in the S37A ß-catenin group, corroborating the higher Wnt activity in this group. Overall design: Two group comparison

Publication Title

Spatially Restricted Stromal Wnt Signaling Restrains Prostate Epithelial Progenitor Growth through Direct and Indirect Mechanisms.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon SRP016518
The expression analyses of metafemales compared with normal females
  • organism-icon Drosophila melanogaster
  • sample-icon 43 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

Comapare the global expression of metafemales and normal femalems Overall design: Collected the metafemales, females and males and made RNA-seq

Publication Title

Dosage compensation and inverse effects in triple X metafemales of Drosophila.

Sample Metadata Fields

Sex, Subject

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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