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SRP093256
Homo sapiens
8 Downloadable Samples
Illumina HiSeq 2000
Description
Purpose: NGS has revolutionized systems-based analysis of cell signaling pathways. The goal of this study is to determine the effects of PPARD in colon cancer cell transcriptomes in relation to the metastatic potential. Methods: NGS-derived colon cancer cell mRNA transcriptome profiles of HCT116 WT (HCT116) and HCT116 with genetic PPARD-knockout (KO1) cells were generated by deep sequencing, in quadruplicate, using Illumina HiSeq2000 .The transcriptomes of HCT116 and KO1 cells will be compared to determine the differentially expressed genes between HCT116 and KO1 cells. Differentially expressed genes will be examined in relation to the metastatic potential and validated by qRT-PCR. Results: Using an optimized data analysis workflow Tophat2, we mapped about 25 million sequence reads per sample to the human genome. Out of 22229 genes, we identified 12118 transcripts with >50 reads in at least one sample of HCT116 and KO1 cells with edgeR package and identified 6668 differentailly expressed genes with FDR 0.001 and P value cutoff 0.0022 using GLM tests fitted with BUM model. We further fltered the genes with both p-value and fold change and identified 416 genes with FDR 0.001 and fold change larger than 2. Among the differentially expressed genes, 311 were downregulated and 105 were upregulated in the KO1 cells compared with the WT cells. Twenty-three of the differentially expressed genes had significant association (i.e., a tendency towards co-occurrence) with PPARD expression (P < 0.05; log odds ratio > 1.5) in the TCGA colorectal adenocarcinoma database. Of these 23 genes, 7 were linked to metastasis by PubMed literature searches: GJA1, VIM, SPARC, NRG1, CXCL8 (IL-8), STC1, and SNCG, which were validated by q-RT-PCR. Conclusions: Our study represents the detailed analysis of PPARD transcriptomes in colon cancer cells, generated by mRNA-seq technology. Our results show that NGS offers a comprehensive and accurate quantitative and qualitative evaluations of mRNA contents in cells. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions. Overall design: The transcriptome profiles of HCT116 WT and KO1 colon cancer cells were generated by deep sequencing, in quadruplicate, using Illumina HiSeq2000.
Publication Title
Metastasis regulation by PPARD expression in cancer cells.
Sample Metadata Fields
Subject
View Samples- Homo sapiens
- 3 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Array-based gene expression, CGH and tissue data defines a 12q24 gain in neuroblastic tumors with prognostic implication.
Sample Metadata Fields
Sex, Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 3 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Title: Array-based gene expression, CGH and tissue data define a 12q24 gain in neuroblastic tumors with prognostic implication.
Publication Title
Array-based gene expression, CGH and tissue data defines a 12q24 gain in neuroblastic tumors with prognostic implication.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Mus musculus
- 36 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
The Y chromosome as a regulatory element shaping immune cell transcriptomes and susceptibility to autoimmune disease.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Understanding the DNA elements that constitute and control the regulatory genome is critical for the appropriate therapeutic management of complex diseases. Here, using chromosome Y (ChrY) consomic mouse strains on the C57BL/6J background, we show that susceptibility to two diverse animal models of autoimmune disease, including experimental allergic encephalomyelitis (EAE) and experimental myocarditis, correlates with the natural variation in copy number of Sly and Rbmy multicopy ChrY genes. In the B6 background, ChrY possesses gene regulatory properties that impact both genome-wide gene expression and the presence of alternative splice variants in pathogenic CD4+ T cells. Using a ChrY consomic strain on the SJL background, we discovered a preference for ChrY-mediated gene regulation in macrophages, the immune cell subset underlying the EAE sexual dimorphism in SJL mice, rather than CD4+ T cells. Importantly, in both genetic backgrounds, an inverse correlation exists between the number of Sly and Rbmy ChrY gene copies and the number of significantly upregulated genes in immune cells, thereby supporting a link between copy number variation of Sly and Rbmy with the ChrY genetic element exerting regulatory properties. Moreover, in humans, an analysis of the CD4+ T cell transcriptome from male multiple sclerosis patients versus healthy controls provides further evidence for an evolutionarily conserved mechanism of gene regulation by ChrY. Thus, these data establish ChrY as a member of the regulatory genome in mammals due to its ability to regulate gene expression and alternative splicing in immune cells linked to disease.
Publication Title
The Y chromosome as a regulatory element shaping immune cell transcriptomes and susceptibility to autoimmune disease.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Understanding the DNA elements that constitute and control the regulatory genome is critical for the appropriate therapeutic management of complex diseases. Here, using chromosome Y (ChrY) consomic mouse strains on the C57BL/6J background, we show that susceptibility to two diverse animal models of autoimmune disease, including experimental allergic encephalomyelitis (EAE) and experimental myocarditis, correlates with the natural variation in copy number of Sly and Rbmy multicopy ChrY genes. In the B6 background, ChrY possesses gene regulatory properties that impact both genome-wide gene expression and the presence of alternative splice variants in pathogenic CD4+ T cells compared to CD4+ T cells. An inverse correlation exists between the number of Sly and Rbmy ChrY gene copies and the number of significantly upregulated genes in immune cells, thereby supporting a link between copy number variation of Sly and Rbmy and the ChrY genetic element exerting regulatory properties. Thus, these data establish ChrY as a member of the regulatory genome in mammals due to its ability to regulate gene expression and alternative splicing in immune cells linked to disease.
Publication Title
The Y chromosome as a regulatory element shaping immune cell transcriptomes and susceptibility to autoimmune disease.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 26 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Huntingtons disease (HD) is a neurodegenerative disorder that is associated with the deposition of proteinaceous aggregates in the brains of HD patients and mouse models. Previous studies have suggested that wide-scale disruption of protein homeostasis occurs in protein folding diseases. Protein homeostasis can be maintained by activation of the heat shock response (HSR) via the transcription factor heat shock factor 1 (HSF1), the pharmacological activation of which can be achieved by Hsp90 inhibition and has been demonstrated to be beneficial in cell and invertebrate models of HD. Whether the HSR is functional in HD and whether its activation has therapeutic potential in mammalian HD models is currently unknown. To address these issues, we used a novel, brain penetrant Hsp90 inhibitor to activate the HSR in brain after systemic administration. Microarrays, quantitative PCR and western blotting showed that the HSR becomes impaired with disease progression in two mouse models of HD and that this originates at the level of transcription.
Publication Title
Altered chromatin architecture underlies progressive impairment of the heat shock response in mouse models of Huntington disease.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment
View Samples- Drosophila melanogaster
- 60 Downloadable Samples
- Illumina HiSeq 2500
Description
CbtOE (Tim-gal4; UAS-cbtFLAG), Tim-gal4 (control for CbtOE), cbtRNAi (Tim-gal4-UAS-Dcr2-UAS-cbtIR-cbtE1) and Tim-gal4;UAS-Dcr2 (control for CbtRNAi) flies. Flies were entrained in LD (light: dark) condition for 3-4 days and harvested at six time points: ZT3, ZT7, ZT11, ZT15, ZT19, ZT23 Fly heads were collected, RNA was extracted and RNA-seq libraries were prepared as previously described (Engreitz et al., 2013) Overall design: Three samples of cbtRNAi and three samples of their controls. Two samples of cbtOE with two samples of their controls.
Publication Title
The transcription factor Cabut coordinates energy metabolism and the circadian clock in response to sugar sensing.
Sample Metadata Fields
Specimen part, Subject, Time
View Samples- Drosophila melanogaster
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
Control (+/cbtE1-UAS-cbt RNAi) or cabut RNAi flies (Tim-gal4, UAS-cbt RNAi) were starved for 16 hours and then exposed to food containing different concentrations of sucrose: 0, 25, 50 and 100 % for 18 hours. Fly heads were collected, RNA was extracted and RNA-seq libraries were prepared as previously described (Engreitz et al., 2013) Overall design: For each sucrose concentration, two samples of cabut RNAi flies and one sample of control flies were sequenced.
Publication Title
The transcription factor Cabut coordinates energy metabolism and the circadian clock in response to sugar sensing.
Sample Metadata Fields
Specimen part, Subject
View Samples- Drosophila melanogaster
- 6 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
Microarray data obtained from control, cbtRNAi (cabut RNAi), and cbtOE (cabut overexpression) flies. From each strain, fly heads at two different time points during the daynight cycle (ZT3 and ZT153) were collected.
Publication Title
The transcription factor Cabut coordinates energy metabolism and the circadian clock in response to sugar sensing.
Sample Metadata Fields
Specimen part, Treatment
View Samples