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GSE13432
Mus musculus
12 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Cold triggers VEGF dependent but hypoxia independent angiogenesis in adipose tissues and anti-VEGF agents modulate adipose metabolism
Publication Title
Hypoxia-independent angiogenesis in adipose tissues during cold acclimation.
Sample Metadata Fields
Sex
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Vascular pericytes, an important cellular component, in the tumor microenvironment, are often associated with tumor vasculatures and their functions in cancer invasion and metastasis are poorly understood. Here we show that PDGF-BB induces pericyte fibroblast transition (designated as PFT), which significantly contributes to tumor invasion and metastasis. Gain- and loss-of-function experiments demonstrate that the PDGF-BB-PDGFR signaling promotes PFT in vitro and in in vivo tumors. Genome-wide expression analysis indicates that PDGF-BB-activated pericytes acquire mesenchymal progenitor features. Pharmacological inhibition and genetic deletion of PDGFR ablate the PDGF-BB-induced PFT. Genetic tracing of pericytes with two independent mouse strains, i.e., TN-AP-CreERT2:R26R-tdTomato and NG2:R26R-tdTomato, shows that PFT cells gains stromal fibroblast and myofibroblast markers in tumors. Importantly, co-implantation of PFT cells with less-invasive tumor cells in mice markedly promotes tumor dissemination and invasion, leading to an increased number of circulating tumor cells (CTCs) and metastasis. Our findings reveal a novel mechanism of vascular pericytes in PDGF-BB-promoted cancer invasion and metastasis by inducing PFT and thus targeting PFT may offer a new treatment option of cancer metastasis.
Publication Title
Pericyte-fibroblast transition promotes tumor growth and metastasis.
Sample Metadata Fields
Specimen part
View Samples- Saccharomyces cerevisiae
- 47 Downloadable Samples
Illumina HiSeq 2000
Description
Epigenetic mechanisms including histone post-translational modifications control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging aspect of shortened lifespan, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a lifespan screen in S. cerevisiae, designed to identify altered amino acid residues of histones that alter yeast replicative aging. Our results reveal that lack of sustained H3K36 methylation is commensurate with increased cryptic transcription in a set of genes in old cells and shorter lifespan. Deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes and suppresses cryptic transcript initiation to extend lifespan. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to an increase in transcriptional noise that is detrimental to lifespan, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity. Overall design: This study examines transcription in yeast aging using a WT or Rph1 mutant background over a sequence of time-dependent FACS sorts of old cells. Cryptic transcripts are detected using a small fragment sequencing approach. The youngest WT yeast (designated S1Y, S2Y) are represented in seven biological replicates and one technical replicate, five small fragment and three others; the oldest WT yeast (designated S4O) are also represented in seven biological replicates and one technical replicate, again composed of five small fragment samples and three others. Intermediate WT yeast aging sorts (S2O and S3O) are each represented by five biological replicates and one technical replicate, three small fragment and three others. For mutant yeast, each stage in the time series is represented by five biological replicates and one technical replicate, three small fragment and three others. Experiment 4 is a technical replicate of experiment 3.
Publication Title
H3K36 methylation promotes longevity by enhancing transcriptional fidelity.
Sample Metadata Fields
Subject
View Samples- Caenorhabditis elegans
- 4 Downloadable Samples
- NextSeq 500
Description
Epigenetic mechanisms including histone post-translational modifications control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging aspect of shortened lifespan, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a lifespan screen in S. cerevisiae, designed to identify altered amino acid residues of histones that alter yeast replicative aging. Our results reveal that lack of sustained H3K36 methylation is commensurate with increased cryptic transcription in a set of genes in old cells and shorter lifespan. Deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes and suppresses cryptic transcript initiation to extend lifespan. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to an increase in transcriptional noise that is detrimental to lifespan, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity. Overall design: This study examines transcription in worm aging using FUDR treatment. The samples represent a time-series, with one control group without FUDR, and then three treated with FUDR at days 1, 8, and 12. Days 8 and 12 represent old worms. There are no replicates.
Publication Title
H3K36 methylation promotes longevity by enhancing transcriptional fidelity.
Sample Metadata Fields
Cell line, Treatment, Subject
View Samples- Homo sapiens
- 2 Downloadable Samples
- Illumina HiSeq 4000
Description
High-throughput sequencing was employed to analyze the genes whose expression are altered when lncRNA LAST is downregulated by shRNA in HCT116 cells. The Gencode Gene ID of lncRNA LAST is ENSG00000254682.1. Overall design: In order to identify the genes whose expression levels were changed under the condition of LAST knockdown, we performed High-throughput sequencing and mRNA expression profile data analyzing.
Publication Title
<i>LAST</i>, a c-Myc-inducible long noncoding RNA, cooperates with CNBP to promote <i>CCND1</i> mRNA stability in human cells.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 58 Downloadable Samples
- IlluminaGenomeAnalyzerII, IlluminaGenomeAnalyzer
Description
Noncoding RNAs (ncRNAs) are emerging as key molecules in human cancer, with the potential to serve as novel markers of disease and to reveal uncharacterized aspects of tumor biology. Here we discover 121 unannotated prostate cancer–associated ncRNA transcripts (PCATs) by ab initio assembly of high-throughput sequencing of polyA+ RNA (RNA-Seq) from a cohort of 102 prostate tissues and cells lines. We characterized one ncRNA, PCAT-1, as a prostate-specific regulator of cell proliferation and show that it is a target of the polycomb repressive complex 2 (PRC2). We further found that patterns of PCAT-1 and PRC2 expression stratified patient tissues into molecular subtypes distinguished by expression signatures of PCAT-1–repressed target genes. Taken together, our findings suggest that PCAT-1 is a transcriptional repressor implicated in a subset of prostate cancer patients. These findings establish the utility of RNA-Seq to identify disease-associated ncRNAs that may improve the stratification of cancer subtypes. Overall design: 21 prostate cell lines sequenced on the Illumina Genome Analyzer and GAII. Variable number of replicates per sample. RNA-Seq data from prostate cancer tissues used in this study will be made available on dbGAP.
Publication Title
Transcriptome sequencing across a prostate cancer cohort identifies PCAT-1, an unannotated lincRNA implicated in disease progression.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 43 Downloadable Samples
- Illumina HiSeq 2500
Description
Systemic sclerosis (SSc) is a devastating disease affecting the skin and internal organs. Dermal fibrosis manifests early and Modified Rodnan Skin Scores (MRSS) correlate with disease progression. Transcriptomics of SSc skin biopsies suggest the role of the in vivo microenvironment in maintaining the pathological myofibroblasts. Therefore, defining the structural changes in dermal collagen in SSc patients could inform our understanding of fibrosis pathogenesis. Here, we report a method for quantitative whole-slide image analysis of dermal collagen from SSc patients, and our findings of more aligned dermal collagen bundles in diffuse cutaneous SSc (dcSSc) patients. Using the bleomycin-induced mouse model of SSc, we identified a distinct high dermal collagen bundle alignment gene signature, characterized by a concerted upregulation in cell migration, adhesion, and guidance pathways, and downregulation of spindle, replication, and cytokinesis pathways. Furthermore, increased bundle alignment induced a cell migration gene signature in fibroblasts in vitro, and these cells demonstrated increased directed migration on aligned ECM fibers that is dependent on expression of Arhgdib (Rho GDP-dissociation inhibitor 2). Our results indicate that increased cell migration is a cellular response to the increased collagen bundle alignment featured in fibrotic skin. Moreover, many of the cell migration genes identified in our study are shared with human SSc skin and may be new targets for therapeutic intervention. Overall design: For bleomycin experiments, 8 week old C57Bl/6 female mice were used.The bleomycin model was established with daily subcutaneous injections of bleomycin (100uL at 1U/mL) into the back skin. Experimental timepoints include: saline, 2 weeks bleo, 4 weeks bleo, 6 weeks recovery, and 10 weeks recovery.
Publication Title
Increased dermal collagen bundle alignment in systemic sclerosis is associated with a cell migration signature and role of Arhgdib in directed fibroblast migration on aligned ECMs.
Sample Metadata Fields
No sample metadata fields
View Samples- Arabidopsis thaliana
- 36 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Tailoring high-density oligonucleotide arrays for transcript profiling of different Arabidopsis thaliana accessions using a sequence-based approach.
Sample Metadata Fields
Specimen part
View Samples- Arabidopsis thaliana
- 18 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
In order to identify differentially expressed genes in developing seeds of Arabidopsis thaliana three different stages of seed development were analysed (9-10, 10-11 and 12-13 days after flower opening) for two Arabidopsis thaliana accessions, Col-0 and C24. For each stage and accession three biological replicates were analysed.
Publication Title
Tailoring high-density oligonucleotide arrays for transcript profiling of different Arabidopsis thaliana accessions using a sequence-based approach.
Sample Metadata Fields
Specimen part
View Samples- Arabidopsis thaliana
- 18 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
In order to identify differentially expressed genes in developing seeds of Arabidopsis thaliana three different stages of seed development were analysed (9-10, 10-11 and 12-13 days after flower opening) for two Arabidopsis thaliana accessions, Col-0 and C24. For each stage and accession three biological replicates were analysed.
Publication Title
Tailoring high-density oligonucleotide arrays for transcript profiling of different Arabidopsis thaliana accessions using a sequence-based approach.
Sample Metadata Fields
Specimen part
View Samples