Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE78025 | GEO | 2020/04/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome analysis reveals malignant and hypoxic signature of glioblastoma

Project description:Purpose:Glioblastoma (GBM) is the most common primary brain tumor in adults with poor prognosis and short medial survival after therapy. 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 normoxia and 1% O2 hypoxia for transcriptional profiling to gain further insight into the molecular underpinnings that maintained the properties of GBM andclarify the molecular mechanism of hypoxia resistance of GBM. 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 normoxia and 1% O2 hypoxia for transcriptional profiling. And validating the analysis results with specimens of GBM patients. Results: Firstly, the resulting data set revealed previously unknown proteins, including AKR1B1, MT2A, UBC, EEF1A1 and MTRNR2l2 in U87-MG cells, which promoted GBM characters through MAPK pathway. Meanwhile, we found that toll-like pathway was a new avenue mediating the function of inflammatory response in GBM. Furthermore, The results suggested that cytokine TGF-β1 and HIFs’ targeted genes, including HMOX1 and STC1 could be regard as hypoxic markers for GBM. Conclusion:Taken together, our study identified new potential biomarkers and illustrated the genes associated with inflammation in GBM. More importantly, the unique pattern to hypoxia implied new insight for the GBM research of hypoxia resistance and recurrence in future.

2019-09-11 | GSE77307 | 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 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

Hypoxia-induced circPLOD2a/b promote migration and invasion of GBM cells via suppressing XIRP1 through binding to HuR [2]

Project description:Background. Glioblastoma (GBM) is the most lethal form of brain tumors in human adults, and hypoxia is a common microenvironment in this disease. Circular RNAs (circRNAs) are identified as regulators in cancers including GBM. However, the specific roles of circRNAs in GBM under hypoxic condition remains elusive. Methods. RNA-seq was employed to investigate the expression profile of circRNAs in U87 cells under normoxia and hypoxia. Two circRNAs spliced from the same parental gene, named as circPLOD2a and circPLOD2b, were identified as hypoxia-responsive circRNAs, whose circular structures were verified by, qRT-PCR, RNase R digesting and Sanger sequencing in U87. Knockdown and overexpression of circPLOD2a/b in GBM cells were used to investigate the biological functions of these two circRNAs on tumor progression. Fluorescence in situ hybridization, RNA-pull down, mass spectrometry and RNA immunoprecipitation assays were conducted to explore the interactions between circPLOD2a/b, human antigen R (HuR), xin actin binding repeat containing 1 (XIRP1). Results. CircPLOD2a/b were significantly up-regulated in hypoxic GBM cells and directly induced by HIF1α under hypoxia. Overexpression of circPLOD2a/b enhance GBM cell invasion and migration, which could be inhibited by circPOD2a/b knockdown. Mechanistically, circPLOD2a/b competitively bind to HuR, inhibiting the interaction between HuR and XIRP1, thus promoting the tumor aggressiveness in GBM both in vitro and in vivo through down-regulating XIRP1. Conclusions. Hypoxia-induced circPLOD2a/b were identified as key regulators of migration and invasion in GBM cells, and act as oncogenic circRNAs to attenuate the interaction between HuR and XIRP1, which may be potential therapeutic strategy for GBM treatment.

2023-10-23 | GSE245635 | GEO

Hypoxia-induced circPLOD2a/b promote migration and invasion of GBM cells via suppressing XIRP1 through binding to HuR [1]

2023-10-23 | GSE245634 | GEO

Allopregnanolone alters the gene expression profile of human glioblastoma cells

Project description:Glioblastomas (GBM) are one of the most frequent and aggressive brain tumors. In these malignancies, progesterone (P4) promotes proliferation, migration, and invasion. The P4 metabolite allopregnanolone (3α-THP) similarly promotes cell proliferation in the U87 human GBM cell line. Here, we evaluated global changes in gene expression of U87 cells treated with 3α-THP, P4, and the 5α-reductase inhibitor, finasteride (F).

2018-02-11 | GSE108998 | GEO

DNA methylation characterisation of glioblastoma (GBM) cell lines.

Project description:Early passages (< 10) of frequently used GBM cell lines A172, LN18, LN229, T98G, U87-MG, U138-MG and U251-MG were characterised for global DNA methylation patterns.

2023-07-01 | GSE119592 | GEO

Gene expression analysis of glioblastoma (GBM) cell lines.

Project description:Early passages (< 10) of frequently used GBM cell lines A172, LN18, LN229, T98G, U87-MG, U138-MG and U251-MG were characterised for gene expression microarray analysis.

2023-07-01 | GSE119468 | GEO

Genomic copy number number characterisation of glioblastoma (GBM) cell lines.

Project description:Early passages (< 10) of frequently used GBM cell lines A172, LN18, LN229, T98G, U87-MG, U138-MG and U251-MG were characterised for genomic copy number by array CGH.

2023-07-01 | GSE119586 | GEO

Uncovering small non-coding RNAs involved in carcinogenesis of Glioma

Project description:To determine which signalling pathways are affected by small RNAs (piRNAs, miRNAs) through target regulation in Glioblastoma Multiforme (GBM), we performed high-throughput next-generation sequencing in U87-MG GBM cell line. The RNA sequencing (RNA-Seq) of small RNAs and transcriptomes discovered both known and novel piRNAs and miRNAs as well other transcriptomes of protein-coding genes, lncRNAs and pseudogenes expressed in this GBM cell line. These small RNAs and target transcriptomes can be further investigated to decode novel molecular mechanisms underlying oncogenesis of this malignancy.

2023-04-04 | GSE197508 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data