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Transcriptome analysis reveals malignant and hypoxic signature of glioblastoma

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE77307 | GEO | 2019/09/11

REPOSITORIES: GEO

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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

Expression data from Glioma-Initiating Cells (GICs) cultured under hypoxia and normoxia

Project description:Glioblastoma (GBM) is the most common and aggressive primary brain tumor in adults, with glioma initiating cells (GICs) implicated to be critical for tumor progression and resistance to therapy. The hypoxic tumor microenvironment has been shown to play an important role to maintain the GICs; however, the mechanisms regulating responses of GICs to hypoxia remain poorly understood. We used microarray to to detail the global change of gene expression in GICs cultured under hypoxia compared to normoxia and identified de-regulated genes during hypoxia. CD133+ D456MG GICs were cultured under 1% O2 or 20% O2 for 12 hours. Then RNA was extracted and gene expression was profiled by microarray.

2016-07-03 | E-GEOD-73556 | biostudies-arrayexpress

Gene expression data in A172 cell line transfected with Anti-miR-196a-5p miRNA or its respective negative control under hypoxia (0.2% O2)

Project description:miR-196a-5p is robustly upregulated under hypoxia in GBM cell lines and is highly expressed in GBM tumour samples. This study identifies the genes differentially expressed upon miR-196a-5p inhibition in A172 glioblastoma cell line under hypoxia (0.2% O2). GeneChip PrimeView Human Gene Expression Array was used to assess mRNA expression profile in response to miR-196a-5p inhibition in A172 cell line under hypoxia (0.2% O2).

2020-12-15 | GSE152575 | GEO

Expression profiling of hypoxic HepG2 hepatoma, U87 glioma, and MDA-MB231 breast cancer cells: time course

Project description:Analysis of expression changes of cultured HepG2 hepatoma, U87 glioma, and MDA-MB231 breast cancer cells subjected to hypoxia (0.5% O2) for 0, 4, 8, 12 hours . Results provide insight to cell type-specific response to hypoxia. HepG2 hepatoma, U87 glioma, and MDA-MB231 breast cancer cells were collected under normoxic conditions (~19% O2, 0 hours) and after 4, 8 and 12 hours of hypoxia treatment (0.5% O2). For each cell line, three replicates of total RNA at each time point were prepared using Trizol and submitted to the DFCI Microarray Core for labeling, hybridization to Affymetrix HG-U133Plus2 oligonucleotide arrays and image scanning.

2010-06-21 | E-GEOD-18494 | biostudies-arrayexpress

Analysis of gene expression changes in response to hypoxia and/or cisplatin in A2780 and A2780cis cells

Project description:The aim of this experiment was to evaluate the changes in gene expression in response to hypoxia and/or cisplatin in an ovarian cancer cell line model. A2780 (cisplatin-sensitive) and A2780cis (cisplatin-resistant) cell lines were treated with cisplatin in normoxia or hypoxia (0.5% O2) for 72 hours. RNA was extracted from three independent biological replicates for each condition: A2780 (normoxia, untreated); A2780 (hypoxia, untreated); A2780 (normoxia, cisplatin); A2780cis (hypoxia, cisplatin), A2780cis (normoxia, untreated); A2780cis (hypoxia, untreated); A2780cis (normoxia, cisplatin); A2780cis (hypoxia, cisplatin) and interrogated on Affymetrix Human Gene ST 1.0 arrays.

2016-01-15 | E-MTAB-3645 | biostudies-arrayexpress

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

Identification of genes activated in cancer cells cultured under hypoxia and serum-free condition

Project description:To identify genes activated under hypoxia (1%O2) and serum-free treatment of a cancer cell line, we performed cDNA microarray analysis with an ovarian cancer cell line, OVSAYO. Cells were cultured under normoxia /hypoxia (1%O2) and serum-plus/serum-minus conditions for 16 hours. Total RNA was isolated for cDNA microarray analysis.

2015-04-01 | E-GEOD-55564 | biostudies-arrayexpress

Transcription profiling of human hypoxia exposed normal human esophageal epithelial cells

Project description:To delineate the role of hypoxia in esophageal epithelial biology, we carried out gene array experiments using a non-transformed immortalized diploid human esophageal cell line, EPC2-hTERT (Mol Cancer Res. 2003;1:729-38). Unlike cancer cell lines, EPC2-hTERT has no genetic alterations at early passages that may affect the cellular response to hypoxia. Experiment Overall Design: EPC2-hTERT cells were exposed to moderate (1% O2) hypoxia in experiment 1 (Exp1) or severe (0.2% O2) hypoxia in experiment 2 (Exp2). Normoxia (21% O2) served as a control in both experiments.

2009-09-12 | E-GEOD-17353 | biostudies-arrayexpress

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