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Next Generation Sequencing Facilitates Quantitative Analysis of U87 Transcriptomes to define the ALKBH5-dependent hypoxia-induced genes

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of U87 Transcriptomes to define the ALKBH5-dependent hypoxia-induced genes

PROVIDER: PRJNA718825 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14118873.fastq.gz	Fastqsanger.gz
	SRR14118874.fastq.gz	Fastqsanger.gz
	SRR14118875_1.fastq.gz	Fastqsanger.gz
	SRR14118875_2.fastq.gz	Fastqsanger.gz
	SRR14118876_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Next Generation Sequencing Facilitates Quantitative Analysis of U87 Transcriptomes to define the ALKBH5-dependent hypoxia-induced genes

Project description:Among 720 hypoxia-induced genes (at least 2 folds of upregulation in Hypoxia-treated U87 WT or shScr cells compared with Normoxia), the expression of 35 genes is significantly suppressed by ALKBH5 depletion (U87 Hypoxia shALKBH5/shScr)

2024-03-31 | GSE171227 | GEO

Hypoxia and ALKBH5 in U87 cells

Project description:Hypoxia and ALKBH5 in U87 cells

| PRJNA719809 | ENA

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

m6A methylation regulates hypoxia-induced pancreatic cancer glycolytic metabolism through ALKBH5-HDAC4-HIF1α positive feedback loop

Project description:To study the effects of hypoxia-related m6A modification which were mediated by ALKBH5 in pancreatic cancer, we established the ALKBH5 knockdown cell lines in PANC-1 cells. And then, the ALKBH5 knockdown cell lines were cultured under hypoxia for 48 h.

2023-09-08 | GSE218546 | GEO

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

Project description:Compared with the normoxia control, 174 m6A peaks from 58 m6A-modified transcripts are significantly increased while 2032 m6A peaks from 556 m6A-modified transcripts are significantly decreased in hypoxia. Among the downregulated m6A peaks in hypoxia compared with normoxia condition, ALKBH5 depletion leads to 847 increased m6A peaks in 276 transcripts (fold change≥1.5).

2024-03-31 | GSE171497 | 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

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

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

| PRJNA728459 | ENA

ALKBH5 is a New Mammalian RNA Demethylase

Project description:N6-methyladenosine (m6A) is the most prevalent internal modification of messenger RNA (mRNA) in higher eukaryotes. Here we report ALKBH5 as a new mammalian demethylase that oxidatively removes the m6A modification in mRNA in vitro and inside cells. This demethylation activity of ALKBH5 significantly affects mRNA export and RNA metabolism as well as the assembly of mRNA processing factors in nuclear speckles. Alkbh5-deficient male mice are characterized by impaired fertility resulting from apoptosis that affects meiotic metaphase-stage spermatocytes. In accordance with this defect, we have identified in mouse testes 1552 differentially expressed genes which cover broad functional categories and include spermatogenesis-related mRNAs involved in the p53 functional interaction network. We show that Alkbh5-deficiency impacts the expression levels of some of these mRNAs, supporting the observed phenotype. The discovery of this new RNA demethylase strongly suggests that the reversible m6A modification plays fundamental and broad functions in mammalian cells. RNA-seq in two cell types

2013-02-15 | E-GEOD-40132 | biostudies-arrayexpress

ALKBH5 Induces Fibroblast-to-Myofibroblast Transformation During Hypoxia to Protect Against Cardiac Rupture After Myocardial Infarction

Project description:Objectives: To investigate the role of ALKBH5 in fibroblasts during post-myocardial infarction (MI) repair. Background: N6-methyladenosine (m6A) mRNA modification has been shown to play an important role in cardiovascular diseases. The RNA demethylase, AlkB homolog 5 (ALKBH5), is an m6A "eraser" that is responsible for decreased m6A methylation. However, its role in cardiac fibroblasts during the post-MI healing process remains elusive. Methods: MI was mimicked by permanent left anterior descending artery ligation in global ALKBH5-knockout, ALKBH5-knockin, and fibroblast-specific ALKBH5-knockout mice to study the function of ALKBH5 during post-MI collagen repair. Methylated RNA immunoprecipitation sequencing was performed to explore potential ALKBH5 targets. Results: Dramatic alterations in ALKBH5 expression were observed during the early stage post-MI and in hypoxic fibroblasts. Global ALKBH5 knockin reduced infarct size and improved cardiac function after MI. The global and fibroblast-specific ALKBH5-knockout mice both exhibited low survival rates along with poor collagen repair, impaired cardiac function, and cardiac rupture. Both in vivo and in vitro ALKBH5 loss led to impaired fibroblast activation and decreased collagen deposition. Additionally, hypoxia, but not TGF-β1 or Ang II, upregulated ALKBH5 expression in myofibroblasts in a HIF-1α-dependent transcriptional manner. Mechanistically, ALKBH5 promoted the stability of ErbB4 mRNA and the degradation of ST14 mRNA via m6A demethylation. Fibroblast-specific ErbB4 overexpression ameliorated the impaired fibroblast-to-myofibroblast transformation and poor post-MI repair due to ALKBH5 knockout. Conclusions: Fibroblast ALKBH5 positively regulates post-MI healing via post-transcriptional modification and stabilization of ErbB4 mRNA in an m6A-dependent manner. Targeting ALKBH5/ERBB4 may be a potential therapeutic option for post-MI cardiac rupture.

2023-10-01 | GSE226415 | GEO

Genome-wide HIF-1, RNA polII, and H3K4me3 binding sites in U87 and HepG2 cells

Project description:Hypoxia-Inducible Factor 1 (HIF-1) plays a key role in cellular adaptation to hypoxia. To better understand the determinants of HIF-1 binding and transactivation, we used ChIP-chip and gene expression profiling to define the relationship between the epigenetic landscape, sites of HIF-1 binding, and genes transactivated by hypoxia in two cell lines, HepG2 hepatoma cell line and U87 glioma cell line.

2009-10-09 | GSE18499 | GEO

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