Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA312377 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3175550_1.fastq.gz | Fastqsanger.gz | |||
| SRR3175550_2.fastq.gz | Fastqsanger.gz | |||
| SRR3175541_1.fastq.gz | Fastqsanger.gz | |||
| SRR3175541_2.fastq.gz | Fastqsanger.gz | |||
| SRR3175551_1.fastq.gz | Fastqsanger.gz |
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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
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
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
Project description:Four human mesenchymal stem cells (hMSC) clones (MSC-1, MSC-2, MSC-3, MSC-4) and three different glioblastoma multiformae (GBM) cell lines (U87-MG, U251, U373) were used to study their mutual paracrine interactions in the indirect co-cultures compared to their monocultures, which were grown under the same experimental conditions. The effects on cell growth, proliferation and invasion in matrigel were quantified. Further on, bioinformatic tools were used to relate these results to the data obtained from cytokine macroarrays and DNA microarrays that revealed proteins and genes significantly involved in the interaction. We showed that hMSC are responsible for the impairment of GBM cell invasion and growth, possibly via induction of their senescence. On the other hand, U87-MG cells even more strongly inversely affected some of these characteristics in hMSCs. We found several chemokines that may account for changed co-cultured cells’ phenotype, affecting genes associated with proliferation and senescence. CCL2/MCP-1 was collectively identified as the most significantly regulated chemokine during hMSC and U87-MG paracrine signalling. Its role in U87-MG cell invasion was also functionally confirmed. Microarray data deposited here contain gene expression data from three biological replicates of monocultures and indirect co-cultures of MSC-4 and U87-MG cells, representing 12 microarrays. Three biological replicates of four cell set-ups were performed: MSC-4 monoculture, U87-MG monoculture, MSC-4 co-cultured with U87-MG (in Boyden chambers) and U87-MG co-cultured with MSC-4 (in Boyden chambers).
2011-12-20 | E-GEOD-26283 | biostudies-arrayexpress
Project description:Four human mesenchymal stem cells (hMSC) clones (MSC-1, MSC-2, MSC-3, MSC-4) and three different glioblastoma multiformae (GBM) cell lines (U87-MG, U251, U373) were used to study their mutual paracrine interactions in the indirect co-cultures compared to their monocultures, which were grown under the same experimental conditions. The effects on cell growth, proliferation and invasion in matrigel were quantified. Further on, bioinformatic tools were used to relate these results to the data obtained from cytokine macroarrays and DNA microarrays that revealed proteins and genes significantly involved in the interaction. We showed that hMSC are responsible for the impairment of GBM cell invasion and growth, possibly via induction of their senescence. On the other hand, U87-MG cells even more strongly inversely affected some of these characteristics in hMSCs. We found several chemokines that may account for changed co-cultured cells’ phenotype, affecting genes associated with proliferation and senescence. CCL2/MCP-1 was collectively identified as the most significantly regulated chemokine during hMSC and U87-MG paracrine signalling. Its role in U87-MG cell invasion was also functionally confirmed. Microarray data deposited here contain gene expression data from three biological replicates of monocultures and indirect co-cultures of MSC-4 and U87-MG cells, representing 12 microarrays.
2011-12-20 | GSE26283 | GEO
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
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
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
Project description:PD-L1 Inhibitor Regulates the miR-33a-5p/PTEN Signaling Pathway and Can Be Targeted to Sensitize Glioblastomas to Radiation. Glioblastoma (GBM) is the most common and lethal brain tumor in adults. Ionizing radiation (IR) is a standard treatment for GBM patients and results in DNA damage. However, the clinical efficacy of IR is limited due to therapeutic resistance. The programmed death ligand 1 (PD-L1) blockade has a shown the potential to increase the efficacy of radiotherapy by inhibiting DNA damage and repair responses. The miR-33a-5p is an essential microRNA that promotes GBM growth and self-renewal. In this study, we investigated whether a PD-L1 inhibitor (a small molecule inhibitor) exerted radio-sensitive effects to impart an anti-tumor function in GBM cells by modulating miR-33a-5p. U87 MG cells and U251 cells were pretreated with PD-L1 inhibitor. The PD-L1 inhibitor-induced radio-sensitivity in these cells was assessed by assaying cellular apoptosis, clonogenic survival assays, and migration. TargetScan and luciferase assay showed that miR-33a-5p targeted the phosphatase and tensin homolog (PTEN) 3' untranslated region. The expression level of PTEN was measured by western blotting, and was also silenced using small interfering RNAs. The levels of DNA damage following radiation was measured by the presence of γ-H2AX foci, cell cycle, and the mRNA of the DNA damage-related genes, BRCA1, NBS1, RAD50, and MRE11. Our results demonstrated that the PD-L1 inhibitor significantly decreased the expression of the target gene, miR-33a-5p. In addition, pretreatment of U87 MG and U251 cells with the PD-L1 inhibitor increased radio-sensitivity, as indicated by increased apoptosis, while decreased survival and migration of GBM cells. Mir-33a-5p overexpression or silencing PTEN in U87 MG and U251 cells significantly attenuated PD-L1 radiosensitive effect. Additionally, PD-L1 inhibitor treatment suppressed the expression of the DNA damage response-related genes, BRCA1, NBS1, RAD50, and MRE11. Our results demonstrated a novel role for the PD-L1 inhibitor in inducing radio- sensitivity in GBM cells, where inhibiting miR-33a-5p, leading to PTEN activated, and inducing DNA damage was crucial for antitumor immunotherapies to treat GBM.
2020-04-21 | E-MTAB-9007 | biostudies-arrayexpress
Project description:Background: Glioblastoma (GBM) is an aggressive primary brain tumor with poor prognosis and limited treatments. Interferon-gamma (IFN-γ) plays a complex role in modulating immune and tumor responses, and its long-term impact on GBM remains unclear. Methods: Human GBM cell lines U87 and U251 were subjected to up to 28 days of chronic IFN-γ exposure and assessed for morphology, gene expression, protein dynamics, and cytokine secretion. RNA sequencing, automated Western blotting, and single-cell proteomics were employed to uncover distinct cellular and molecular adaptations to prolonged IFN-γ signaling. Results: Chronic IFN-γ exposure induced significantly divergent phenotypic changes in U87 and U251 cells. U87 cells formed neurosphere-like structures and upregulated STAT1/STAT3 signaling, suggesting an immunogenic response. In contrast, U251 cells displayed elongated morphologies and activated PI3K-Akt and Erk pathways, promoting survival and immune evasion. Differential gene expression analysis highlighted unique temporal profiles, with U251 cells exhibiting higher expression of immune resistance genes such as PD-L1 and VEGF. Secretome profiling further demonstrated contrasting cytokine landscapes: U87 cells secreted pro-inflammatory cytokines, while U251 cells produced immunosuppressive factors. Conclusions: Chronic IFN-γ exposure drives distinct molecular and phenotypic changes in GBM subtypes, reflecting their intrinsic heterogeneity. While IFN-γ enhances immune activation, prolonged exposure may also promote immune escape. These findings emphasize the need for therapeutic strategies combining IFN-γ with immune checkpoint inhibitors and targeted pathway modulation to optimize GBM treatment outcomes.
2025-08-12 | GSE304761 | GEO