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accession-icon GSE11114
Comparison of murine masticatory and limb skeletal muscle
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Distinctions between craniofacial and axial muscles exist from the onset of development and throughout adulthood. The masticatory muscles are a specialized group of craniofacial muscles that retain embryonic fiber properties throughout adulthood, suggesting that the developmental origin of these muscles may govern a pattern of expression that differs from limb muscles. To determine the extent of these differences, expression profiling of total RNA isolated from the masseter and tibialis anterior (TA) muscles of adult female mice was performed, which identified transcriptional changes in unanticipated functional classes of genes in addition to those associated with fiber type. In particular, the masseters displayed a reduction of transcripts associated with load-sensing and anabolic processes, and heightened expression of genes associated with stress. Consistent with these observations were a significantly smaller fiber cross-sectional area in masseters, significantly elevated load-sensing signaling (phosphorylated Focal Adhesion Kinase (FAK)), and increased apoptotic index in masseters compared to TA muscles. Based on these results, we hypothesize that masticatory muscles may sense and respond to load differently than limb muscles, where the drive for anabolic processes is reduced, and cell stress mediated processes are enhanced. These results establish a novel classification for the masseter muscle in the spectrum of skeletal muscle allotypes, and may provide insight into the molecular basis for specific muscle-related pathologies associated with masticatory muscles.

Publication Title

Expression profiling reveals heightened apoptosis and supports fiber size economy in the murine muscles of mastication.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon E-MEXP-1288
Transcription profiling of mouse masseter and tibialis anterior muscles to determine expression differences between muscle groups
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Masseter and Tibialis anterior muscles from adult female control mice to determine expression differences between muscle groups

Publication Title

Expression profiling reveals heightened apoptosis and supports fiber size economy in the murine muscles of mastication.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP174478
Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Hepatic iron overload is a risk factor for progression of hepatocellular carcinoma (HCC), although the molecular mechanisms underlying this association have remained unclear. We now show that the iron-sensing ubiquitin ligase FBXL5 is previously unrecognized oncosuppressor in liver carcinogenesis in mice. Hepatocellular iron overload evoked by FBXL5 ablation gives rise to oxidative stress, tissue damage, inflammation and compensatory proliferation in hepatocytes and to consequent promotion of liver carcinogenesis induced by exposure to a chemical carcinogen. The tumor-promoting effect of FBXL5 deficiency in the liver is also operative in a model of virus-induced HCC. FBXL5-deficient mice thus constitute the first genetically engineered mouse model of liver carcinogenesis induced by iron overload. Dysregulation of FBXL5-mediated cellular iron homeostasis was also found to be associated with poor prognosis in human HCC, implicating FBXL5 plays a significant role in defense against hepatocarcinogenesis. Overall design: Total RNA was extracted from the nontumor and tumor tissue of an Alb-Cre/Fbxl5F/F male mouse (nontumor, n = 5; tumor, n = 5) or two littermate control Fbxl5F/F mice (nontumor, n = 6; tumor, n = 6) at 45 weeks of age.

Publication Title

Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE24574
Expression data from BCL6-YFP-positive Tfh cells, BCL6-YFP-negative Tfh cells, non-Tfh cells, and nave helper T cells.
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We found that a number of Tfh cells downmodulated BCL6 protein after their development, and we sought to compare the gene expression between BCL6-hi Tfh cells and BCL6-low Tfh cells.

Publication Title

Bcl6 protein expression shapes pre-germinal center B cell dynamics and follicular helper T cell heterogeneity.

Sample Metadata Fields

Specimen part

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accession-icon SRP092107
RNA-sequencing in TGF-beta treated MDA-231-D cells transfected with ZEB1/ZEB2 siRNAs [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

We searched for roles of ZEB1 during EMT by RNA-seq in breast cancer cells. Overall design: Expression of mRNA in a basal type breast cancer cell line MDA-231-D transfected with ZEB1/ZEB2 siRNAs and stimulated with TGF-beta for 24 h.

Publication Title

ZEB1-regulated inflammatory phenotype in breast cancer cells.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon GSE23153
Gene expression in TNF treated rat aortic rings cultured in collagen or fibrin gels.
  • organism-icon Rattus norvegicus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Angiogenesis in cultures of rat aorta begins with neovessels sprouting from the aortic explant within the first three days of culture.

Publication Title

Macrophage-derived tumor necrosis factor-alpha is an early component of the molecular cascade leading to angiogenesis in response to aortic injury.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE63571
Identification of Gene Regulation Pattern from Lung Cancer Human Tissues
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

To identify individual genes with potential diagnostic and therapeutic utilities in lung cancer, we performed gene expression profiling out of a broad coverage of human transcriptome using clinical patient tissues. Six RNA samples extracted from five cancerous tissues and one normal control were subjected to Affymetrix gene array analysis using Human Exon 1.0 ST Array. Data were further processed using Expression Console and Transcriptome Analysis Console softwares. Both core-gene expression analysis and extended-gene expression analysis were performed to discover significantly regulated genes associated with lung cancer progression.

Publication Title

Discovery of Gene Regulation Pattern in Lung Cancer by Gene Expression Profiling Using Human Tissues.

Sample Metadata Fields

Age

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accession-icon GSE23152
Gene expression during first day of collagen gel culture of rat aortic rings
  • organism-icon Rattus norvegicus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Angiogenesis in collagen gel cultures of rat aorta begins with neovessels sprouting from the aortic explant within the first three days of culture.

Publication Title

Macrophage-derived tumor necrosis factor-alpha is an early component of the molecular cascade leading to angiogenesis in response to aortic injury.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon SRP092615
Time course of mesenchymal breast cancer cells (MT?ECad) undergoing transdifferentiation into terminally differentiated adipocytes
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

A high degree of cell plasticity seems to promote malignant tumour progression, and an epithelial-mesenchymal transition (EMT) is suspected to provide cancer cells with increased cell plasticity for the development of metastasis and therapy resistance. Here, we have tested whether the EMT-induced cancer cell plasticity can be therapeutically exploited and we report the efficient conversion of breast cancer cells, which have undergone an EMT, into post-mitotic adipocytes. Delineation of the molecular pathways underlying such transdifferentiation has motivated a combination therapy with a MEK inhibitor and Rosiglitazone to demonstrate the conversion of invasive cancer cells into adipocytes and the repression of primary tumor invasion and metastasis formation in mouse models of breast cancer. The results indicate the high potential to utilize the increased cell plasticity of invasive cancer cells for differentiation therapy and they raise the possibility to employ pharmacological treatments to interfere with tumor invasion and metastasis. Overall design: Mesenchymal breast cancer cells (MT?ECad) were harvested at six different time-points during trasndifferentiation into terminally differentiated adipocytes (two biological replicates per time-point)

Publication Title

Gain Fat-Lose Metastasis: Converting Invasive Breast Cancer Cells into Adipocytes Inhibits Cancer Metastasis.

Sample Metadata Fields

Subject, Time

View Samples
accession-icon SRP158054
Py2T long term cells and mesenchymal breast cancer cells (MT?ECad) treated with different inhibitors
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Cancer cell plasticity facilitates the development of therapy resistance and malignant progression. De-differentiation processes, such as an epithelial-mesenchymal transition (EMT), are known to enhance cellular plasticity. Here, we demonstrate that cancer cell plasticity can be exploited therapeutically by forcing the trans-differentiation of EMT-derived breast cancer cells into post-mitotic and functional adipocytes. Delineation of the molecular pathways underlying such trans-differentiation has motivated a combination therapy with a MEK inhibitor and the anti-diabetic drug Rosiglitazone in various mouse models of murine and human breast cancer in vivo. This combination therapy provokes the conversion of invasive and disseminating cancer cells into post-mitotic adipocytes leading to the repression of primary tumor invasion and metastasis formation Overall design: Py2T long term cells and mesenchymal breast cancer cells (MT?ECad) were harvested at day7 and treated with different inhibitors (two biological replicates per time-point)

Publication Title

Gain Fat-Lose Metastasis: Converting Invasive Breast Cancer Cells into Adipocytes Inhibits Cancer Metastasis.

Sample Metadata Fields

Specimen part, Treatment, Subject, Time

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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