Genomic maps of TUG1 and gene expression profiling in human glioma stem cell
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ABSTRACT:
PROVIDER: PRJNA275381 | ENA |
REPOSITORIES: ENA
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Project description:Glioblastomas show heterogeneous histological features. These distinct phenotypic states are thought to be originated by the glioma stem cells (GSCs), which are highly tumorigenic and self-renewing sub-population of tumor cells that have different functional characteristics. We found TUG1, a large non-coding RNA (lncRNA) is highly expressed in GSCs. TUG1 was reported to interact with PRC2 via its exon 2 and represses its target gene expression in trans. In order to identify the genetic loci enriched with TUG1 in GSC, we performed modified RNA pull-down assay coupled with promoter-microarray analysis using BrU-labeled TUG1.
2016-11-23 | GSE65910 | GEO
Project description:Glioblastomas show heterogeneous histological features. These distinct phenotypic states are thought to be associated with the presence of glioma stem cells (GSCs), which are highly tumorigenic and self-renewing sub-population of tumor cells that have different functional characteristics. We found that TUG1, a long non-coding RNA (lncRNA), plays pivotal roles in maintaining the self-renewal properties of GSC. Some lncRNAs are known to act as a miRNA sponge in the cytoplasm, where lncRNAs bind to miRNAs and quench their activity. To investigate miRNA expression profiling in GSC upon TUG1 inhibition, we have performed microarray experiment using SurePrint G3 Human miRNA 8x60K Microarray (G4872A, Agilent Technologies).
2016-11-23 | GSE79896 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2016-11-23 | GSE65911 | GEO
Project description:The evolutionary conserved Taurine Upregulated Gene 1 (TUG1) is a ubiquitously expressed gene that is one of the highest expressed genes in human and rodent endothelial cells (ECs). We here show that TUG1 expression decreases significantly in aging mouse carotid artery ECs and human ECs in vitro, indicating a potential role in the aging endothelial vasculature system. We therefore investigated if, and how, TUG1 might function in aging ECs, but despite extensive phenotyping found no alterations in basal EC proliferation, apoptosis, barrier function, migration, mitochondrial function, or monocyte adhesion upon TUG1 silencing in vitro. TUG1 knockdown did slightly and significantly decrease cumulative sprout length upon vascular endothelial growth factor A stimulation in human umbilical vein endothelial cells (HUVECs), though TUG1-silenced HUVECs displayed no transcriptome-wide mRNA expression changes explaining this effect. Further, ectopic expression of the highly conserved and recently discovered 153 amino acid protein translated from certain TUG1 transcript isoforms did not alter angiogenic sprouting in vitro. Our data show that, despite a high expression and strong evolutionary conservation of both the TUG1 locus and the protein sequence it encodes, TUG1 does not seem to play a major role in basic endothelial cell function.
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Project description:We report maps of H3K4me3 and H3ac - activiting expression histone modifications in C6 rat glioma cells. The data was obtained using whole genome high throughput technology. The sequencing was performed on HiSeq Ilumina platform. Examination of H3K4me3 histone modification and H3ac histone modification in C6 rat glioma cell line
2015-05-07 | E-GEOD-46820 | biostudies-arrayexpress
Project description:We have sequenced mouse embryonic fibroblasts (MEFs) and 6 organs (testes, prostate, liver, heart, spleen, and eye) harvested from adult male wild type and Tug1 knockout (Tug1_tm1.1Vlcg) mice in a C57BL/6J/129S6 (N3-C57BL/6J, no Neo) background. Additional sequencing was done on the testes of a Tug1 rescue mouse, which contains a doxycycline inducible allele for Tug1 (tg(Tug1)) and CAGs-rtTA3 in the Tug1 knockout background (Tug1_tmn1.1Vlcg).
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Project description:Gene expression profiling and genome-wide maps in PDGFB-induced glioma
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Project description:We generated a genome wide map of instances where the long noncoding RNA, Tug1, binds to DNA in cultured mouse podocytes under normal glucose conditions using Chromatin-RNA Precipitation coupled with high throughput sequencing (ChIRP-Seq) 48 alternating (even, odd) biotynilated probes were designed to span the full length of Tug1 RNA. Chromatin was prepared from gluteraldehyde crosslinked nuclei from early passage podocytes. Chromatin extracts were duplicated with either even or odd probes. Duplicate samples for Input DNA, Even pulldown (PD) and Odd PD DNA was purified following incubation and supplied for Illumina sequencing by ArrayStar (Rockville, MD).
2016-10-24 | E-GEOD-77493 | biostudies-arrayexpress
Project description:Hepatocellular carcinoma (HCC) remains the third leading cause of cancer deaths; however, its therapeutic options are limited. Understanding the molecular mechanisms of HCC could shed light on new therapies. Emerging studies indicate the important role of long-noncoding RNAs (lncRNAs) in the pathogenesis of HCC. One of the early discovered lncRNAs, taurine-upregulated gene 1 (TUG1), has been up-regulated in HCC tissues, but its impact on HCC cells’ transcriptomics remains unexplored. We established TUG1-knockdown HCC cells and performed RNA-seq analysis. KEGG analysis revealed the significant enrichment of downregulated genes involved in glycolysis. Accordingly, TUG1-depleted HCC cells showed impairments in glucose uptake, ATP synthesis, and lactate production. Clinical HCC tissue data revealed positive gene expression correlations between TUG1 and glycolysis genes identified by RNA-seq. To identify a molecular function of TUG1 in glycolysis, we explored the competing endogenous (ceRNA) model and identified five microRNAs (miRNAs) with the highest number of TUG1 binding sites using bioinformatic tools. Amongst these miRNAs, microRNA-122-5p (miR-122-5p) displayed an inverse relationship for gene expression with most TUG1-regulated glycolysis genes, including PKM, ALDOA, ENO2, and PFKM. Dual luciferase assays confirmed the direct interaction between TUG1 and miR-122-5p and between miR-122-5p and the 3’ untranslated regions (3’UTR) of PKM and ALDOA. We further showed that inhibition of miR-122-5p alleviated the suppression of glycolysis induced by TUG1 depletion. Together, our RNA-seq analysis of TUG1-depleted HCC cells in combination with clinical data reveals the crucial function of TUG1 in promoting glycolysis via sponging miR-122-5p, which is a negative regulator of multiple glycolytic enzymes.
2025-07-29 | GSE273253 | GEO