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accession-icon GSE90922
Expression data in JDCaP prostate cancer xenograft model before and after expression of AR splice variants
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Our previous study using nude rats revealed that the parental JDCaP xenografts predominantly expressed full-length androgen receptor (AR) whereas the relapsed JDCaP xenografts after castration acquired AR splice variants including AR-V7 and ARv567es. To understand molecular mechanisms underlying the acquisition of AR splice variants in the JDCaP model, we performed microarray analysis using RNA samples of the xenografts without castration (Parent), the relapsed xenografts overexpressing full-length AR and AR-V7 (ARhiV7hi), and the relapsed xenografts expressing ARv567es (ARv567es).

Publication Title

The RNA helicase DDX39B and its paralog DDX39A regulate androgen receptor splice variant AR-V7 generation.

Sample Metadata Fields

Specimen part

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accession-icon GSE68837
Expression data from cell lines forced expressed PGC7/Stella
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Global DNA hypomethylation and DNA hypermethylation of promoter regionsincluding tumor suppressor genesare frequently detected in human cancers. Although many studies have suggested a contribution to carcinogenesis, it is still unclear whether the aberrant DNA hypomethylation observed in tumors is a consequence or a cause of cancer. We found that overexpression of Stella (also known as PGC7, Dppa3), a maternal factor required for the maintenance of DNA methylation in early embryos, induced global DNA hypomethylation and transformation in NIH3T3 cells. This hypomethylation was due to the binding of Stella to Np95 (also known as Uhrf1, ICBP90) and the subsequent impairment of Dnmt1 localization. In addition, enforced expression of Stella enhanced the metastatic ability of B16 melanoma cells through the induction of metastasis-related genes by inducing DNA hypomethylation of their promoter regions. Such DNA hypomethylation itself causes cellular transformation and metastatic ability. These data provide new insight into the function of global DNA hypomethylation in carcinogenesis.

Publication Title

Global DNA hypomethylation coupled to cellular transformation and metastatic ability.

Sample Metadata Fields

Cell line

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accession-icon SRP032537
Transcriptome of Nkx2-5-null atria
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer

Description

Atrial specific knockout of Nkx2-5 results in hyperplastic atria with ASD and conduction defects. To examine how Nkx2-5 regulates cardiac proliferation at late gestational stages, RNA-seq was performed. Overall design: Examination of expression profile of 2 Nkx2-5-null atria and 3 controls

Publication Title

Nkx2-5 suppresses the proliferation of atrial myocytes and conduction system.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE33171
Gene expression comparison between two human cancer cell Lines: Oral squamous cell carcinoma SASL1m and adenoid cystic carcinoma ACC2
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

SASL1 is highly metastatic to lymph nodes. ACC2 is not metastatic. We compared gene expression on cultured cells to identify genes associated to metastatic spread patterns.

Publication Title

Premetastatic vasculogenesis in oral squamous cell carcinoma xenograft-draining lymph nodes.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE40260
Microarray using CD31+/CD41-/CD45- cells from E9.5 mouse heart tube, caudal half and yolk sac
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Hematopoietic cells arise from spatiotemporally restricted domains in the developing embryo. Although studies of non-mammalian animal and in vitro embryonic stem cell models suggest a close relationship among cardiac, endocardial, and hematopoietic lineages, it remains unknown whether the mammalian heart tube serves as a hemogenic organ akin to the dorsal aorta. Here, we examined the hemogenic activity of the developing endocardium. Mouse heart explants generated myeloid and erythroid colonies in the absence of circulation. Hemogenic activity arose from a subset of endocardial cells in the outflow cushion and atria earlier than in the aorta-gonad-mesonephros region, and was transient and definitive in nature. Interestingly, key cardiac transcription factors, Nkx2-5 and Isl1, were expressed in and required for the hemogenic activity of the endocardium. Together, these data suggest that a subset of endocardial and yolk sac endothelial cells expressing cardiac markers serve as a de novo source for transient definitive hematopoietic progenitors.

Publication Title

Haemogenic endocardium contributes to transient definitive haematopoiesis.

Sample Metadata Fields

Specimen part

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accession-icon GSE138587
Target genes of miR-361-3p in human oral squamous cell carcinoma cells, GFP-SAS
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U219 Array (hgu219)

Description

Inhibition of miR-361-3p by locked nucleic acid (LNA)/DNA antisense oligonucleotide markedly suppressed the growth of GFP-SAS cells.

Publication Title

MicroRNA-361-3p is a potent therapeutic target for oral squamous cell carcinoma.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE42693
Comparative study of sesame lignans affecting gene expression profile and fatty acid oxidation in rat liver
  • organism-icon Rattus norvegicus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

The impact of sesamin, episesamin and sesamolin (sesame lignans) on hepatic gene expression profiles was compared with a DNA microarray. Male Sprague-Dawley rats were fed experimental diets containing 0.2% sesamin, episesamin or sesamolin, and a control diet free of lignans for 15 d. Compared to a lignan-free diet, a diet containing sesamin, episesamin and sesamolin caused 1.5- and 2-fold changes in the expression of 128 and 40, 526 and 152, and 516 and 140 genes, respectively. The lignans modified not only the mRNA levels of many enzymes involved in hepatic fatty acid oxidation, but also those of proteins involved in the transportation of fatty acids into hepatocytes and their organelles, and regulate hepatic concentrations of carnitine, CoA and malonyl-CoA. It is apparent that sesame lignans stimulate hepatic fatty acid oxidation by affecting the gene expression of various proteins regulating hepatic fatty acid metabolism. We also observed that lignans modified the gene expression of various proteins involved in hepatic lipogenesis, cholesterogenesis and glucose metabolism. The changes were generally greater with episesamin and sesamolin than with sesamin. In terms of the amounts accumulated in serum and the liver, the lignans ranked in the order sesamolin, episesamin and sesamin. The differences in bio-availability among these lignans appear to be important to their divergent physiological activities.

Publication Title

Comparative study of sesame lignans (sesamin, episesamin and sesamolin) affecting gene expression profile and fatty acid oxidation in rat liver.

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP157558
Identification of differentially expressed genes between male and female in mouse embryonic fibroblasts (MEFs).
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

The transcriptomic profiles of mouse embryonic fibroblasts (MEFs) were investigated using the next-generation RNA sequencing (RNA-Seq). The CLC Genomic Workbench software was used to screen the differentially expressed transcripts. A total of 49 genes with a significantly differential expression (false discovery rate (FDR) p<0.05, fold change >2) in the female group as compared with the male group. Overall design: mRNA profiles of mouse embryonic fibroblast (MEF) were generated by RNA sequencing using the NextSeq 500 (Illumina).

Publication Title

KDM5D-mediated H3K4 demethylation is required for sexually dimorphic gene expression in mouse embryonic fibroblasts.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon GSE67922
Noncanonical Pathway for Regulation of CCL2 Expression by an mTORC1-FOXK1 Axis Promotes Recruitment of Tumor-Associated Macrophages
  • organism-icon Homo sapiens
  • sample-icon 14 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

C-C chemokine ligand 2 (CCL2) plays pivotal roles in tumor formation, progression, and metastasis. Although CCL2 expression has been found to be dependent on the nuclear factor (NF)B signaling pathway, the regulation of CCL2 production in tumor cells has remained unclear. We have identified a noncanonical pathway for regulation of CCL2 production that is mediated by mammalian target of rapamycin complex 1 (mTORC1) but independent of NF-B. Multiple phosphoproteomics approaches identified the transcription factor forkhead box K1 (FOXK1) as a downstream target of mTORC1. Activation of mTORC1 induces dephosphorylation of FOXK1 resulting in transactivation of the CCL2 gene. Inhibition of the mTORC1-FOXK1 axis attenuated insulin-induced CCL2 production as well as the accumulation of tumor-associated monocytes-macrophages and tumor progression in mice. Our results suggest that FOXK1 directly links mTORC1 signaling and CCL2 expression in a manner independent of NF-B, and that CCL2 produced by this pathway contributes to tumor progression.

Publication Title

Noncanonical Pathway for Regulation of CCL2 Expression by an mTORC1-FOXK1 Axis Promotes Recruitment of Tumor-Associated Macrophages.

Sample Metadata Fields

Cell line

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accession-icon GSE67810
Gene expression alterations by the mTORC1-FOXK1 pathway
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

C-C chemokine ligand 2 (CCL2) plays pivotal roles in tumor formation, progression, and metastasis. Although CCL2 expression has been found to be dependent on the nuclear factor (NF)B signaling pathway, the regulation of CCL2 production in tumor cells has remained unclear. We have identified a noncanonical pathway for regulation of CCL2 production that is mediated by mammalian target of rapamycin complex 1 (mTORC1) but independent of NF-B. Multiple phosphoproteomics approaches identified the transcription factor forkhead box K1 (FOXK1) as a downstream target of mTORC1. Activation of mTORC1 induces dephosphorylation of FOXK1 resulting in transactivation of the CCL2 gene. Inhibition of the mTORC1-FOXK1 axis attenuated insulin-induced CCL2 production as well as the accumulation of tumor-associated monocytes-macrophages and tumor progression in mice. Our results suggest that FOXK1 directly links mTORC1 signaling and CCL2 expression in a manner independent of NF-B, and that CCL2 produced by this pathway contributes to tumor progression.

Publication Title

Noncanonical Pathway for Regulation of CCL2 Expression by an mTORC1-FOXK1 Axis Promotes Recruitment of Tumor-Associated Macrophages.

Sample Metadata Fields

Cell line

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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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