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accession-icon GSE71939
Expression data of SHSY5Y cells after cocaine exposure
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The aim of the study was to evaluate cocaine-induced changes in gene expression in a dopaminergic model.

Publication Title

Transcriptomic and genetic studies identify NFAT5 as a candidate gene for cocaine dependence.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE134614
Expression data from betalains treated C. elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 11 Downloadable Samples
  • Technology Badge IconAffymetrix C. elegans Gene 1.1 ST Array

Description

Effects of betalains in C. elegans gene expression is studied, as our previous results showed a lifespan extension effect produced by theses molecules

Publication Title

Betalain health-promoting effects after ingestion in Caenorhabditis elegans are mediated by DAF-16/FOXO and SKN-1/Nrf2 transcription factors.

Sample Metadata Fields

Age, Specimen part, Treatment

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accession-icon GSE11632
Transcriptional profiling of Tmprss6-deficient mouse liver
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Matriptase-2 (Tmprss6), a recently described member of the TTSP family, is an essential regulator of iron homeostasis. Tmprss6-/- mice display an overt phenotype of alopecia and a severe iron deficiency anemia. These hematological alterations found in Tmprss6-/- mice are accompanied by a marked up-regulation of hepcidin, a negative regulator of iron export into plasma.

Publication Title

Membrane-bound serine protease matriptase-2 (Tmprss6) is an essential regulator of iron homeostasis.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE41799
Transcriptional profiling of human cancer cell lines upon ZMPSTE24 silencing
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Defining the aging-cancer relationship is a challenging task. Mice deficient in Zmpste24, a metalloproteinase mutated in human progeria and involved in nuclear prelamin A maturation, recapitulate many features of aging. However, their short lifespan and cell-intrinsic and -extrinsic alterations restrict the application and interpretation of carcinogenesis protocols. To circumvent these limitations we have generated Zmpste24 mosaic mice. Interestingly, these mice develop normally - revealing cell-extrinsic mechanisms are preeminent in progeria- and display decreased incidence of infiltrating oral carcinomas. Moreover, ZMPSTE24 knock-down reduces human cancer cell invasiveness. Our results disclose the ZMPSTE24-prelamin A system as an example of antagonistic pleiotropy on cancer and aging, support the potential of cell-based and systemic therapies for progeria, and highlight ZMPSTE24 as a new anticancer target.

Publication Title

Prelamin A causes progeria through cell-extrinsic mechanisms and prevents cancer invasion.

Sample Metadata Fields

Cell line

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accession-icon SRP055381
Suppression of NAF-1 in Breast Cancer Cells Reduces their Tumorigenicity by Interfering with Cellular Iron Distribution and Metabolism and Ensuing ROS Formation and Apoptosis
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Nutrient autophagy factor 1 (NAF-1) is an iron-sulfur protein found on the outer mitochondrial membrane and the ER. Recent studies highlighted an important role for NAF-1 in regulating autophagy via interaction with BCL-2. We recently reported that the level of NAF-1 is elevated in cancer cells and that NAF-1 is required for tumor growth. Here we report that shRNA suppression of NAF-1 results in the activation of apoptosis in xenograft tumors and cancer cells grown in culture. Suppression of NAF-1 resulted in a depletion in the cytosolic iron pool, facilitated uptake of iron, and accumulation of iron and ROS in mitochondria, a shift to glycolysis and glutaminolysis, and the activation of cellular stress pathways associated with HIF1a, AMPK and mTOR. Suppression of NAF-1 in breast cancer cells appears therefore to reduce their tumorigenicity by interfering with cellular iron distribution and energy metabolism resulting in the activation of apoptosis. Overall design: Examination of the effect of suppression of NAF-1 in the breast cancer cell line MCF-7. Two sample types were analyzed, MCF-7 suppressed for NAF-1 and MCF-7 Empty vector control, three replicates for each.

Publication Title

Activation of apoptosis in NAF-1-deficient human epithelial breast cancer cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE44387
Transcriptomal profiling of C57BL/6 wild type and ER-alpha KO mice fetal mammary gland after fetal exposure to Bisphenol A (BPA) and 17alpha-ethynylestradiol (EE2)
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To examine whether the BPA-induced morphological alterations of the fetal mouse mammary glands are a) associated with changes in mRNA expression reflecting estrogenic actions and/or b) dependent on the estrogen receptor (ER), we compared the transcriptomal effects of BPA and the steroidal estrogen ethinylestradiol (EE2) on fetal mammary tissues of wild type and ER knock-out mice.

Publication Title

Low-dose BPA exposure alters the mesenchymal and epithelial transcriptomes of the mouse fetal mammary gland.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE24810
Dissecting the signalling pathways underlying cellular senescence
  • organism-icon Homo sapiens
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Cellular senescence is a program of irreversible cell cycle arrest that normal cells undergo in response to progressive shortening of telomeres, changes in telomeric structure, oncogene activation or oxidative stress. The underlying signalling pathways, potentially of major clinicopathological relevance, are unknown. A major stumbling block to studying senescence has been the absence of suitable model systems because of the asynchrony of this process in heterogeneous cell populations. To simplify this process many investigators study oncogene-induced senescence due to expression of activated oncogenes where senescence occurs prematurely without telomere attrition and can be induced acutely in a variety of cell types. We have taken a different approach by making use of the finding that reconstitution of telomerase activity by introduction of the catalytic subunit of human telomerase alone is incapable of immortalising all human somatic cells, but inactivation of the p16-pRB and p53-p21 pathways are required in addition. The ability of SV40 large T antigen to inactivate the p16-pRB and p53-p21 pathways has enabled us to use a thermolabile mutant of LT antigen, in conjunction with hTERT, to develop conditionally immortalised human (HMF3A) fibroblasts that are immortal but undergo an irreversible growth arrest when the thermolabile LT antigen is inactivated leading to activation of pRB and p53. When these cells cease dividing, senescence-associated- b-galactosidase activity is induced and the growth-arrested cells have morphological features and express genes in common with senescent cells. Since these cells growth arrest in a synchronous manner they are an excellent starting point for dissecting the pathways that underlie cellular senescence and act downstream of p16-pRB and p53-p21 pathways. We have combined genome-wide expression profiling with genetic complementation to undertake identification of genes that are differentially expressed when these conditionally immortalised human fibroblasts undergo senescence upon activation of the p16-pRB and p53-p21 tumour suppressor pathways.

Publication Title

Activation of nuclear factor-kappa B signalling promotes cellular senescence.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE58792
Effects of soy supplementation on gene expression in breast cancer
  • organism-icon Homo sapiens
  • sample-icon 49 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background There are conflicting reports on the impact of soy on breast carcinogenesis. This study examines the effects of soy supplementation on breast cancer-related genes and pathways. Methods Women (n = 140) with early-stage breast cancer were randomized to soy protein supplementation (n = 70) or placebo (n = 70) for 7 to 30 days, from diagnosis until surgery. Adherence was determined by plasma isoflavones: genistein and daidzein. Gene expression changes were evaluated by NanoString inin pre- and post-treatment tumor tissue. Genome-wide expression analysis was performed on post-treatment tissue. Proliferation (Ki67) and apoptosis (Cas3) were assessed by immunohistochemistry. Results Plasma isoflavones rose in the soy group (two-sided Wilcoxon rank-sum test, P < .001) and did not change in the placebo group. In paired analysis of pre- and post-treatment samples, 21 genes (out of 202) showed altered expression (two-sided Students t-test, P < .05). Several genes including FANCC and UGT2A1 revealed different magnitude and direction of expression changes between the two groups (two-sided Students t-test, P < .05). A high-genistein signature consisting of 126 differentially expressed genes was identified from microarray analysis of tumors. This signature was characterized by overexpression (>2 fold) of cell cycle transcripts, including those which promote cell proliferation, such as FGFR2, E2F5, BUB1, CCNB2, MYBL2, CDK1, and CDC20 (P < .01). Soy intake did not result in statistically significant changes in Ki67 or Cas3. Conclusions Gene expression associated with soy intake and high plasma genistein define a signature characterized by overexpression of FGFR2 and genes that drive cell cycle and proliferation pathways. These findings raise the concerns that in a subset of women soy could adversely affect gene expression in breast cancer.

Publication Title

The effects of soy supplementation on gene expression in breast cancer: a randomized placebo-controlled study.

Sample Metadata Fields

Treatment

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accession-icon SRP044781
Danio rerio Transcriptome
  • organism-icon Danio rerio
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Transcriptome analysis of 12 zebrafish tissues

Publication Title

Gene evolution and gene expression after whole genome duplication in fish: the PhyloFish database.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE92916
Microarray expression data from mouse embryonic stem cells differentiated into Nkx2-1+ lung and thyroid progenitors
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

The in vitro directed differentiation of pluripotent stem cells (PSCs) through stimulation of developmental signaling pathways can generate mature somatic cell types for basic laboratory studies or regenerative therapies.

Publication Title

Pluripotent stem cell differentiation reveals distinct developmental pathways regulating lung- versus thyroid-lineage specification.

Sample Metadata Fields

Treatment

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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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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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