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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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			Action	DRS
	SRR14475437_1.fastq.gz	Fastqsanger.gz
	SRR14475437_2.fastq.gz	Fastqsanger.gz
	SRR14475438_1.fastq.gz	Fastqsanger.gz
	SRR14475438_2.fastq.gz	Fastqsanger.gz
	SRR14475439_1.fastq.gz	Fastqsanger.gz

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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

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

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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

m6A epitranscriptomic changes in response to hypoxic condition or ALKBH5 knock-down in U87

Project description:m6A epitranscriptomic changes in response to hypoxic condition or ALKBH5 knock-down in U87

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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

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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.

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