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Genome-wide binding of RNF2 in control and GPR17 knock-down U87-MG cells

ABSTRACT: Genome-wide binding of RNF2 in control and GPR17 knock-down U87-MG cells

PROVIDER: PRJNA728458 | ENA |

REPOSITORIES: ENA

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Genome-wide binding of RNF2 in control and GPR17 knock-down U87-MG cells

Project description:GPR17 over-expression inhibits glioma cell proliferation and induces apoptosis by raising ROS levels, and mechanistically inhibits the transcription of RNF2, leading to reduced histone H2A monoubiquitination. Here, To identify the genes mediating the effects of GPR17 and RNF2 on ROS level, we performed RNA-Seq of WT and U87-GPR17 cells and RNF2 ChIP-Seq of WT and U87-shGPR17 cells.

2022-05-10 | GSE174121 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of U87-PLV03 and U87-GPR17 Transcriptomes

2022-05-10 | GSE174122 | GEO

Expression Profiling: Guanylate Cyclase Soluble Subunit Beta-3 (GUCY1B3) overexpression U87 MG cells

2016-06-15 | GSE83344 | GEO

FGFR3 knock-down

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SPARC knock down

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Expression Profiling: Guanylate Cyclase Soluble Subunit Beta-3 (GUCY1B3) overexpression U87 MG cells

Project description:Total RNA were extracted from Guanylate Cyclase Soluble Subunit Beta-3 (GUCY1B3) overexpression U87 MG stable cell lines and U87 MG cells. Three RNA samples of each of the two cell lines were used for microarray analysis to compare gene expression profile Guanylate Cyclase Soluble Subunit Beta-3 (GUCY1B3) was cloned into pCDNA3.1D/V5-His-TOPO plasmid (Invitrgen) and then transfected into U87 MG (ATCC HTB-1) cells to generate stable overexpression cells. RNA from the stable cell lines and U87 MG were used for microarray

2016-06-15 | E-GEOD-83344 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and TWIST1 knock out U87 xenograft mice transcriptomes

Project description:Purpose:Next-generation sequencing has revolutionized sytems-level celluar pathway analysis. The goals of this study are to compare the U87 cell xenograft GBM mice (U87 cell line) to TWIST1 knock out U87 cell xenograft GBM mice (TWIST1 knock out U87 cell line) using their transcriptomes

2018-05-01 | GSE106159 | GEO

Genome-wide expression profiling after acute radiation doses in recurrent U87-MG cells

Project description:To examine short- and long-term gene expression responses following high dose radiation exposure in vitro with the U87-MG cell line. Samples were examined at 1, 4, 6 or 35 days after irradiation with 8 or 16Gy.

2017-05-22 | GSE56937 | GEO

Acute exposure to graded levels of hypoxia in U87-MG cells: the role of hypoxia in GBM

Project description:Purpose: Hypoxia is a predominant feature in GBM and its microenvironment. It is associated with the tumor growth, progression and resistance to conventional therapy of GBM. We have utilized U87-MG cell line as a human GBM cell model and human brain HEB cell line as non-neoplastic brain cell cultured in different levels of hypoxia for transcriptional profiling to identify the transcriptional signature of U87-MG cells for elucidated the role of hypoxia in GBM phenotype. Methods: We have utilized U87-MG cell line as a human GBM cell model and human brain HEB cell line as non-neoplastic brain cell cultured in 21%, 5% and 1% O2 for 24h. Then we detected the changes of transcriptional profiling and analyzed the biological process and pathway for the genes with different expression modes in different hypoxia levels. Results: U87-MG cells present specific transcriptional signature response to different hypoxia levels. The genes associated with organ and system development present an upward trend from normoxia to extreme hypoxia. And the biological process of DNA repair presents a downward trend, indicating that gene mutations of U87-MG cells could derive by hypoxia microenvironment. Otherwise, HEB cells present the canonical response to hypoxia, reducing of the metabolic rate in concert with the degree of hypoxia and extracting more oxygen from the environment. Conclusion: Hypoxia microenvironment could promote the malignance of GBM through activate of genes involved in organ and system development. Meanwhile it could induce the mutations of genes in GBM, especially extreme hypoxia.

2020-04-01 | GSE78025 | GEO

Hypoxia-responsive gene expression profile of U87 MG glioblastoma cells and their exosomes.

Project description:How cancer cells adapt to hypoxia during tumor development remains an important question. The hypothesis tested in the present study was that tumor cell-derived exosome vesicles (also known as microvesicles or extracellular vesicles) are mediators of hypoxia-dependent intercellular signaling in glioblastoma (GBM), i.e. highly aggressive brain tumors characterized by hypoxia and a vascular density that is among the highest of all human malignancies. In vitro hypoxia experiments and studies with patient materials reveal the enrichment in exosomes of hypoxia-regulated mRNAs and proteins, several of which were associated with poor patient prognosis. We show that cancer cell exosomes mediate hypoxia-dependent, phenotypic modulation of stromal cells in vitro and ex vivo, resulting in accelerated GBM tumor angiogenesis and growth in mice. These data suggest that exosomes constitute potent mediators of hypoxia-driven tumor development, and circulating multiparameter biomarkers of tumor hypoxia. U87 MG glioblastoma cells were grown at normoxic (21% oxygen) or hypoxic (1% oxygen) conditions for 48 hours. Conditioned media from normoxic and hypoxic cells were then used to isolate exosomes by differential centrifugation. Both cells and exosomes were lysed in Trizol reagent, and RNA was isolated.Total RNA from all samples (four types of samples in three biological repilicates) was subjected to genome-wide transcriptional analysis with Illumina HumanHT-12 V3.0 expression beadchip. Gene expression profile obtained from hypoxic U87 MG glioblastoma cells was compared to the profile of normoxic control cells. Analogically, gene expression profile obtained from hypoxic U87 MG cells was compared to the profile of exosomes secreted by normoxic U87 MG cells.

2013-03-20 | E-GEOD-45301 | biostudies-arrayexpress

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