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Detection of transcriptome changes caused by knockdown of Ptbp1 in U251 GBM cells

ABSTRACT: Detection of transcriptome changes caused by knockdown of Ptbp1 in U251 GBM cells

PROVIDER: PRJNA784588 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17066806_1.fastq.gz	Fastqsanger.gz
	SRR17066806_2.fastq.gz	Fastqsanger.gz
	SRR17066807_1.fastq.gz	Fastqsanger.gz
	SRR17066807_2.fastq.gz	Fastqsanger.gz
	SRR17066808_1.fastq.gz	Fastqsanger.gz

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Detection of transcriptome changes caused by knockdown of Ptbp1 in U251 GBM cells

Project description:We demonstrated that knocking down Ptbp1 can reprogram GBM cells into neuron-like cells. In order to further explore the mechanism of Ptbp1 causing this phenomenon, we performed mRNA sequencing on U251 cells infected with sh-Luci-3d, sh-Ptbp1-3d and sh-Ptbp1-7d.

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Detection of transcriptome changes caused by overexpression of NeuroD4 in U251 glioblastoma cells

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HOXA9 transcriptomic analysis in GBM cell lines (U87MG, U251 and primary GBML18) and in immortalized human astrocytes (hTERT/E6/E7)

Project description:Assess gene expression patterns upon HOXA9 ectopic expression in U87MG GBM cell line and hTERT/E6/E7 immortalized human astrocytes, and HOXA9 silencing in U251 and GBML18 GBM cell lines. U87MG and hTERT/E6/E7 were retrovirally-infected with an MSCV control vector (MSCV-Control) or with a construct containing the coding region of HOXA9 (MSCV-HOXA9), resulting in U87MG-Control, U87MG-HOXA9, hTERT/E6/E7-Control and hTERT/E6/E7-HOXA9 cell lines. GBML18 and U251 cells were transfected with HOXA9 gene-specific shRNA sequences (shHOXA9) or a non-efective shRNA (shControl) in pGFP-V-RS plasmid, resulting in U251-shControl, U251-shHOXA9, GBML18-shControl and GBML18-shHOXA9 cell lines. Four experimental replicates for HOXA9 overexpression cell lines, and three for HOXA9 silencing cell lines were performed.

2015-01-30 | E-GEOD-56517 | biostudies-arrayexpress

HOXA9 transcriptomic analysis in GBM cell lines (U87MG, U251 and primary GBML18) and in immortalized human astrocytes (hTERT/E6/E7)

2015-01-30 | GSE56517 | GEO

Detection of transcriptome changes caused by overexpression of NeuroD4 in U251 glioblastoma cells

Project description:Detection of transcriptome changes caused by overexpression of NeuroD4 in U251 glioblastoma cells

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Transcription profiling by array of human U251 cells treated with DMSO or enzastaurin

Project description:We identified GSK3 as a regulator of GBM cell survival using microarray analysis, small molecule and genetic inhibitors of GSK3 activity. Various molecular and genetic approaches were then employed to dissect out the molecular mechanisms responsible for GSK3 inhibition-induced cytotoxicity. Experiment Overall Design: RNA extracted from U251 cells treated with DMSO or Enzastaurin for indicated time were hybridized to Affymetrix expression arrays (HG_U133-Plus_2) to detect changes in gene expression caused by Enzastaurin. Three replicates per sample were used.

2009-01-14 | E-GEOD-11285 | biostudies-arrayexpress

mRNA sequence of the glioma cell line U251 after TEAD3 knockdown

Project description:Glioma is a malignant primary tumour that occurs in the central nervous system. TEA domain transcription factor (TEAD) family proteins are the Hippo pathway's ultimate effector molecules. The function of TEAD3 in gliomas is still unclear. Therefore, RNA sequencing was performed on TEAD3 knockdown U251 cells and normal U251 cells. The samples in this study included normal U251 control group and TEAD3 knockdown group. Each group contained three samples. Total RNA was extracted using Trizol reagent following the manufacturer's procedure. The total RNA quantity and purity were analysis of Bioanalyzer 2100 and RNA 6000 Nano LabChip Kit, high-quality RNA samples with RIN number > 7.0 were used to construct sequencing library. Gene Set Enrichment Analysis (GSEA) based on the sequencing results showed that knockdown of TEAD3 in the U251 cell line caused changes in several important pathways, including CTLA4 inhibitory pathway, defective pyroptosis, signaling by Hippo, regulation of TP53 activity, E2F mediated regulation of DNA replication, and FCGR3A mediated phagocytosis.

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Next Generation Sequencing Analysis of Wild Type (WT) and SRSF1 knockdown (KD) U87MG and U251 cells Transcriptomes

Project description:We generated the SRSF1 knockdown U87MG and U251 cells by infecting with shRNA virus. Then, we extracted RNAs and performed next generation sequencing. By comparing sequencing data from WT and KD samples in each cell type, we profiled the alternative splicing events and gene expression regulated by SRSF1 in GBM.

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Trancriptome profiling of glioma cell line U87 and U251 with LAMP2A knockdown

Project description:The objective of the study was to examine the gene expression changes in glioma cell line U87 and U251 with LAMP2A knockdown. There were 15 samples in total- U87-1, U87-2, U87-3, U87-1812-1, U87-1812-2, U87-1812-3, U251-1, U251-2, U251-3, U251-1812-1, U251-1812-2, U251-1812-3, U251-1813-1, U251-1813-2, and U251-1813-3. U87-1 to U87-3 and U251--1 to U251-3 were used as the control groups (CON). U87-1812-1 to U871812-3, U251-1812-1 to U251-1812-3, and U251-1813-1 to U251-1813-3 were used as the experimental groups (shLAMP2A-1 and shLAMP2A-2). The total RNA of each sample was extracted from the stable transfected glioma cells by using TRIzol reagent. Then the RNA samples were processed for high throughput transcriptome sequencing on Illumina HiSeq 3000 platform. There were two types of libraries: the circRNA, mRNA, and lncRNA were all constructed by removing rRNA (one library, three types of RNA were analyzed together), and the insert fragment was about 300bp; the small RNA was constructed and analyzed separately, mainly microRNA of about 22bp. Results: among 60612 cleaned mRNAs, 781 were differentially expressed in U87-1812 group compared with U87 group, 146 were differentially expressed in U251-1812 group compared with U251 group, 43 were differentially expressed in U251-1813 group compared with U251 group (padj ≤ 0.05 and expression change ≥2 fold). The differential expressed genes distributed in all chromosomes. Functional annotation with GO and KEGG enrichment revealed the top functional groups including inflammation, DNA replication, cell adhesion, TNF, IL17, and axon guidance signaling pathways.

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Transcriptomic analysis of senescent cells upon PTBP1 knockdown.

Project description:IMR90 ER:RAS cells were stably transduced with either an empty vector or 2 deconvoluted shRNAs targeting PTBP1. Following selection with puromycin, the cells were treated with 4OHT to induce senescence. 6 days later the cells were collected for total mRNA analysis. PTBP1 is a regulator of alternative splicing. Our previous experiments had shown that PTBP1 depletion inhibits the expression of pro-inflammatory genes without affecting other senescence-associated phenotypes. By performing RNA-seq we confirmed those observations at a global level and analysed how PTBP1 knockdown alters alternative splicing as a potential mechanism of action.

2018-06-25 | GSE101750 | GEO

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