MRNA expression profiling in human brain glioblastoma cell line U251 after stable knockdown the expression of linc01116
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE103455 | GEO | 2018/08/31
REPOSITORIES: GEO
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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.
2023-01-25 | GSE223378 | GEO
Project description:We showed that DBTRG is more invasive than U251 cell lines by novel brain-stiffness-mimicking matrix gel invasion platform and transwell invasion assay. To understand the molecular mechanisms of DBTRG being more invasive than U251, we performed transcriptomic sequencing analysis of DBTRG and U251 cell lines.
2022-04-18 | GSE200574 | GEO
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| S-ECPF-GEOD-35454 | biostudies-other
Project description:To elucidate the mechanism(s) underlying the synergistic interaction between ETV6 and NFKB1, we analyzed the genome-wide transcriptional consequences of single and double knock-downs of the two TFs in U251 cells.
2016-09-26 | GSE75003 | GEO
Project description:The human TP53 gene is frequently mutated in tumors and cell lines. Unlike other tumor suppressors that are commonly inactivated by deletions or nonsense mutations, the majority of p53-mutations are missense point mutations that result in the expression of a full-length protein with an altered amino acid that has lost sequence specific DNA-binding. Expression of mutant p53 (mutp53) confers advantages to tumor cells and transcriptional regulation of several genes mediating the beneficial effects has been shown to play a role. However, molecular mechanisms of transcriptional regulation by mutp53 are still poorly understood. We used the glioblastoma-derived U-251 MG human cell line endogenously expressing mutp53 protein (R273H mutation) to analyze gene expression profiles on Agilent Whole Human Genome Microarray after transient and stable depletion of mutp53 expression. Gene expression data was correlated with a ChIP study on a custom tiling array to understand the contribution of endogenously expressed mutp53 to transcriptional regulation. This series of microarray experiments contains the gene expression profiles of glioblastoma-derived U-251 MG human cell lines engineered to constitutively express a p53-specific shRNA or scrambled control shRNA. To reverse the effect of mutp53 depletion, stable clones were modified by stable integration of a mutp53-R273H expression construct or empty pCDNA3 vector as a control. In addition, we performed gene expression analysis of U-251 MG cells transiently transfected with p53-specific siRNA or control siRNA (3 biological replicates each).
2012-12-10 | E-GEOD-35454 | biostudies-arrayexpress
Project description:Missense point mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines derived thereof. Mutant p53 (mutp53) proteins have lost sequence-specific DNA binding, but have retained the ability to interact in a structure-selective manner with non-B DNA and to act as regulators of transcription. To identify functional binding sites of mutp53, we established a small library of genomic sequences bound by p53R273H in U251 human glioblastoma cells using chromatin immunoprecipitation (ChIP). Mutp53 binding to isolated DNA fragments confirmed the specificity of the ChIP. The mutp53 bound DNA sequences are rich in repetitive DNA elements, which are dispersed over non-coding DNA regions. Stable down-regulation of mutp53 expression strongly suggested that mutp53 binding to genomic DNA is functional. We identified the PPARGC1A and FRMD5 genes as p53R273H targets regulated by binding to intronic and intra-genic sequences. We propose a model that attributes the oncogenic functions of mutp53 to its ability to interact with intronic and intergenic non-B DNA sequences and modulate gene transcription via re-organization of chromatin. For the study of the consequences of mutant p53 (R273H) knockdown on gene expression, total RNA from parental U251 glioblastoma cells and UsiA12 clone was prepared from two independent cell culture experiments (biological replicates) and processed for microarray-based profiling of gene expression. UsiA12 clone was derived from the U251 cells transfected with the pSuper-p53 and pCI-neo vectors.
2010-06-24 | E-GEOD-13991 | biostudies-arrayexpress
Project description:We identified a rare coding variant (p.K420Q) in the complement component 7 (C7) gene affecting the risk of Alzheimer's disease. To investigate the cellular effects of the mutant, we performed RNA-seq in cell line overexpression wilt-type and mutant C7. U251 glioma cells with stable expression of mutant APP (K670N/M671L) (U251-APP cells), which produce Aβ42 under Dox inducing, were used as the model cell. Total RNA of U251-APP cells overexpressing wild type and mutant C7 proteins were subjected to transcriptome sequencing using Illumina Hiseq 4000 platform.
2018-11-22 | GSE101608 | GEO
Project description:We present RNA-Seq data obtained from U251 control cells and U251 cells with stable overexpression of lncRNA XLOC13218 to identify differentially expressed genes. The discovery of long non-coding RNAs (lncRNAs) has improved the understanding of development and progression in various cancer sub-types. However, the role of lncRNAs in temozolomide (TMZ) resistance in glioblastoma (GBM) remains largely undefined. In this present study, the differential expression of lncRNAs were identified between U87 and U87TR (TMZ-resistant) cells. LncRNA XLOC013218 (XLOC) was drastically upregulated in TMZ-resistant cells and was associated with poor prognosis in glioma. Overexpression of XLOC markedly increased TMZ resistance, promoted proliferation, and inhibited apoptosis in vitro and in vivo. In addition, RNA-seq analysis and gain-of-function or loss-of-function studies revealed that PIK3R2 was the potential target of XLOC. Mechanistically, XLOC recruited Specificity Protein 1 (Sp1) transcription factor and promoted the binding of Sp1 to the promoters of PIK3R2, which elevated the expression of PIK3R2 in both mRNA and protein levels. Finally, PIK3R2-mediated activation of the PI3K/AKT signaling pathway promoted TMZ resistance and cell proliferation, but inhibited cell apoptosis. In conclusion, these data highlight the vital role of XLOC/Sp1/PIK3R2/PI3K/AKT axis in GBM TMZ resistance.
2022-04-05 | GSE200031 | GEO
Project description:Transcriptome (RNA-Seq) of the stable overexpression of lncRNA XLOC013218 U251 cells
| PRJNA822649 | ENA
Project description:Using human U251 glioblastoma cells with endogenous mutp53 expression as a model, we performed a ChIP-chip analysis of mutp53 binding sites on a custom tiling array, coupled with global expression profiling and an analysis of the epigenetic status of mutp53 regulated promoters. Mutp53 binds preferentially, and independent of other transcription factors (e.g. ETS1 and SP1), to G/C-rich DNA stretches around transcriptional start sites (TSS) of many genes. Mutp53-bound regions are frequently located in CpG islands and are highly prone to adopt non-B DNA conformation(s). Analysis of the transcriptional status of mutp53-regulated genes demonstrated that mutp53 generally modulates transcription from active promoters marked by H3K4me3. Based on our data we propose a dual mode model of mutp53 GOF, which includes both stochastic and deterministic components. On a local scale, mutp53 acts as a basal transcriptional co-factor that has the potential to bind autonomously and selectively to non-B DNA structures around TSSs of active genes and to modulate transcription rates of many genes in a context and stimulus-dependent fashion. Resulting stochastic alterations generate transcriptional plasticity and enhance transcriptional competence on a global scale. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2012-12-10 | E-GEOD-35500 | biostudies-arrayexpress