Gene expression profiling of four subpopulations in GBM
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE24244 | GEO | 2010/11/21
SECONDARY ACCESSION(S): PRJNA133019
REPOSITORIES: GEO
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Project description:GBM is a heterogenous brain tumor with hyperproliferation of endothelial cells. In order to understand the cellular mechanism of vasculogenesis in GBM, four fractions of cells are seperated. Microarray assays was performed to examine the potential lineage relationship and the signal pathways involved in determining the cell identity and function. Four subpopulation of cells were seperated from two independent GBM dissociates by FCAS assay based on the expression of membrane marker CD133 and CD144. Total RNA was extracted from freshly sorted cells without any culture.
2010-11-21 | E-GEOD-24244 | biostudies-arrayexpress
Project description:GBM is a heterogenous tumor. Based on membrane protein expression, the GBM single cell dissociates were seperated into different subfractions by FACS assay. The genomic aberration among each populations were compared by analysis of CGH data.
2010-11-21 | GSE24452 | GEO
Project description:GBM is a heterogenous tumor. Based on membrane protein expression, the GBM single cell dissociates were seperated into different subfractions by FACS assay. The genomic aberration among each populations were compared by analysis of CGH data. Genomic DNA were extracted from sorted cell population and CGH assay were performed to compare the similarity genomic abnormality among different cell groups.
2010-11-21 | E-GEOD-24452 | biostudies-arrayexpress
Project description:GBM is a heterogenous brain tumor with hyperproliferation of endothelial cells. In order to understand the cellular mechanism of vasculogenesis in GBM, four fractions of cells are seperated. Microarray assays was performed to examine the potential lineage relationship and the signal pathways involved in determining the cell identity and function. Four subpopulation of cells were seperated from two independent GBM dissociates by FCAS assay based on the expression of membrane marker CD133 and CD144. Total RNA was extracted from freshly sorted cells without any culture.
| S-ECPF-GEOD-24244 | biostudies-other
Project description:This SuperSeries is composed of the following subset Series: GSE24446: Genetic abnormalities in GBM brain tumors GSE24452: Genetic abnormalities in various cell subpopulations of GBM brain tumors GSE24557: Exon-level expression profiles of GBM brain tumors Refer to individual Series
2010-11-21 | E-GEOD-24558 | biostudies-arrayexpress
Project description:We analyzed, by HTA 2.0, the GBM cell lines LN-18, LN-229, and U-87 MG after fluoresence-activated cell sorting (FACS) into ABCB5+ and ABCB5- fractions. Poor prognosis associated with glioblastoma multiforme (GBM) results from tumor resistance to therapy and high rate of recurrence. Compelling evidence suggests this is driven by subpopulations of slow-proliferating cancer stem cells with tumor-initiating potential. ATP-binding cassette member B5 (ABCB5) has been identified as a molecular marker for distinct subsets of chemoresistant tumor-initiating cell populations in diverse human malignancies. In the current study, we examined the potential role of ABCB5 in growth and chemoresistance of GBM. We found ABCB5 to be preferentially expressed in clinical GBM tumors and co-expressed with the stem cell marker CD133 in subpopulations of human GBM cell lines U-87 MG, LN-18 and LN-229. Antibody-mediated functional ABCB5 blockade inhibited proliferation and survival of human GBM cells and sensitized them to temozolomide (TMZ)-induced apoptosis. Likewise, in an in vivo GBM xenograft study in immunodeficient mice, anti-ABCB5 monoclonal antibody treatment inhibited tumor growth and sensitized tumors to TMZ therapy. Mechanistically, we demonstrated that ABCB5 regulates cell cycle checkpoint molecules to revoke drug-induced G2-M arrest and augments drug-mediated cell death. Overall, our data establish ABCB5 as a marker of GBM chemoresistance and point to the potential of ABCB5 targeting in improvement of current GBM therapies.
2020-03-05 | GSE127895 | GEO
Project description:Single RNA-Seq on GBM cells from human GBM sample
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Project description:Glioblastoma multiforme (GBM) is the most aggressive form of brain tumors. Despite radical surgery and radiotherapy supported by chemotherapy, the disease still remains incurable with extremely low median survival rate of 12-15 months from the time of initial diagnosis. The main cause of treatment failure is considered to be the presence of cells that are resistant to such treatment. MicroRNAs (miRNAs) as regulators of gene expression are involved in the tumor pathogenesis, including GBM. MiR-338 is a brain specific miRNA which has been described to target pathways involved in proliferation and differentiation. In our study, miR-338-3p and -5p were differentially expressed in GBM tissue in comparison to non-tumor brain tissue. Overexpression of miR-338-3p with miRNA mimic did not show any changes in proliferation rates in GBM cell lines (A172, T98G, U87MG). On the other hand, pre-miR-338-5p notably decreased proliferation and caused cell cycle arrest. Since radiation is currently the main treatment modality in GBM, we combined overexpression of pre-miR-338-5p with radiation, which led to significantly decreased of cell proliferation, and increased cell cycle arrest and apoptosis in comparison to only irradiated cells. To better elucidate the mechanism of action, we performed gene expression profiling analysis that revealed targets of miR-338-5p being Ndfip1, Rheb, ppp2R5a. These genes have been described to be involved in DNA damage response, proliferation and cell cycle regulation. To our knowledge, this is the first study to describe role of miR-338-5p in GBM and its potential to improve sensitivity of GBM to radiation. Study was performed on three glioblastoma multiforme cell lines A172, T98G and U87MG. This experiment was performed on Affymetrix GeneChip Human Gene ST 1.0 to elucidate the targets of miRNA-338-5p. Cell lines were seeded 24 hours prior transfection. After transfection with pre-miR338-5p or negative control cell were cultured for 24 hours and harvested. RNA was isolated using MirVana miRNA Isolation Kit (Ambion, USA) and checked for RNA integrity by Bioanalyzer 2100 and purity by ratios 260/280>1.8 and 260/230>1.8 by Nanodrop2000.
2015-12-10 | E-GEOD-75789 | biostudies-arrayexpress