Characterizing the epigenome of glioma stem cells (ChIP-Seq)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE92458 | GEO | 2018/02/23
REPOSITORIES: GEO
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Project description:Glioma initiating cells/stem cells exist in the bulk tumor of glioblastoma. This cell population contributes to the frequent resistances toward radiation/chemotherapy, aggressiveness of adult brain cancer and increased recurrence rate. Targeting stem cell population becomes one the most promising and permissive therapeutic strategies. We isolated glioma stem cells from patient-derived xenografts and profiled their epigenomic features, including 4 different DNA marks and 2 enhancer marks, and transcriptome in these in vitro cultured cell lines. Three fetal brain-derived neural stem/progenitors cells were used for comparing the unique and common molecular features in these glioma cancer stem cells.
2018-02-23 | GSE92460 | GEO
Project description:Glioma initiating cells/stem cells exist in the bulk tumor of glioblastoma. This cell population contributes to the frequent resistances toward radiation/chemotherapy, aggressiveness of adult brain cancer and increased recurrence rate. Targeting stem cell population becomes one the most promising and permissive therapeutic strategies. We isolated glioma stem cells from patient-derived xenografts and profiled their epigenomic features, including 4 different DNA marks and 2 enhancer marks, and transcriptome in these in vitro cultured cell lines. Three fetal brain-derived neural stem/progenitors cells were used for comparing the unique and common molecular features in these glioma cancer stem cells.
2018-02-23 | GSE92462 | GEO
Project description:Glioma initiating cells/stem cells exist in the bulk tumor of glioblastoma. This cell population contributes to the frequent resistances toward radiation/chemotherapy, aggressiveness of adult brain cancer and increased recurrence rate. Targeting stem cell population becomes one the most promising and permissive therapeutic strategies. We isolated glioma stem cells from patient-derived xenografts and profiled their epigenomic features, including 4 different DNA marks and 2 enhancer marks, and transcriptome in these in vitro cultured cell lines. Three fetal brain-derived neural stem/progenitors cells were used for comparing the unique and common molecular features in these glioma cancer stem cells.
2018-02-23 | GSE92459 | GEO
Project description:Characterizing the epigenome of glioma stem cells
| PRJNA357621 | ENA
Project description:To identify a novel miRNA that is aberrantly expressed in GICs, we analyzed differences in miRNA expression between the mouse GICs, NSCL61 and OPCL61, showing characteristic features of cancer stem cell, and their parental cells by miRNA microarrays. neural stem cells, glioma-initiating cells (GICs) from neural stem cells, oligodendrocyte precursor cells, glioma-initiating cells (GICs) from oligodendrocyte precursor cells.
2015-04-07 | E-GEOD-61080 | biostudies-arrayexpress
Project description:Glioma initiating cells (GICs) are considered responsible for the therapeutic resistance and recurrence of malignant glioma. To clarify the molecular mechanism of GIC maintenance/differentiation, we established GIC clones from GBM patient tumors having the potential to differentiate into malignant gliomas in mouse intracranial xenograft, and established an in vitro glioma induction system by using serum stimulation. Upon the serum stimulation, the GIC spheres showed increased cellular proliferation, motility, filopodia/lameripodia formation and adhesion to the culture dishes. Simultaneously, the NSC marker proteins such as CD133 and Sox2 were down-regulated, and the astrocyte/glioma marker GFAP and the malignancy marker CD44 dramatically up-regulated. To identify genes/proteins whose expression changes dynamically during the differentiation of GICs into glioma cells, these GICs were subjected to DNA microarray/iTRAQ based integrated proteomics.
2013-01-26 | GSE43762 | GEO
Project description:The recent identification of cancer stem cells (CSCs) in multiple human cancers provides a new inroad to understanding tumorigenesis at the cellular level. CSCs are defined by their characteristics of self-renewal, multipotentiality, and tumor initiation upon transplantation. By testing for these defining characteristics, we provide evidence for the existence of CSCs in a transgenic mouse model of glioma, S100ß-verbB;Trp53. In this glioma model, CSCs are enriched in the side-population (SP) cells. These SP cells have enhanced tumor-initiating capacity, self-renewal, and multipotentiality compared to non-SP cells from the same tumors. Furthermore, gene expression analysis comparing FACS-sorted cancer SP cells to non-SP cancer cells and normal neural SP cells identified 45 candidate genes that are differentially expressed in glioma stem cells. We validated the expression of two genes from this list (S100a4 and S100a6) in primary mouse gliomas and human glioma samples. Analyses of xenografted human GBM (glioblatoma multiforme) cell lines and primary human glioma tissues show that S100A4 and S100A6 are expressed in a small subset of cancer cells and that their abundance is positively correlated to tumor grade. In conclusion, this study shows that CSCs exist in a mouse glioma model, suggesting that this model can be used to study the molecular and cellular characteristics of CSCs in vivo and to further test the cancer stem cell hypothesis.
2008-12-15 | GSE13490 | GEO
Project description:Glioblastoma is a malignant brain tumor that is highly resistant to radiation and chemotherapy, where patients survive on average only 15 months after diagnosis. Furthering the understanding of mechanisms leading to radiation resistance of glioma is paramount to identify novel therapeutic targets. Previous studies have shown that glioma stem cells (GSCs) play an important role in promoting radiation resistance and disease recurrence. Herein we analyze the proteomic alterations occurring in patient-derived GSCs upon radiation treatment in order to identify molecular drivers of resistance. We show that proteome changes upon radiation accurately predict the resistance status of the cells, and that resistance to radiation does not correlate with glioma transcriptional subtypes. We further show that the radio-resistant cell line GSC-267 sheds microvesicles (MVs) enriched in the metabolic enzyme nicotinamide phosphoribosyltransferase (NAMPT).
2023-04-06 | PXD030092 | Pride
Project description:To identify factors involved in tumorigenicity of glioma-initiating cells (GICs), we compared gene expression in GIC-like cells with and without sox11 expression. We established sox11-expressing mouse glioma-initiating cell (GIC)-like cell line (NSCL61s), NSCL61s-sox11, which lost tumorigenicity when transplanted in vivo. We think that genes, which are differently expressed between NSCL61s and NSCL61s-sox11, would be new targets for glioma therapy.
2009-11-30 | E-GEOD-17076 | biostudies-arrayexpress
Project description:One of the most detrimental hallmarks of glioblastoma multiforme (GBM) is cellular invasiveness, considered a potential cause of tumor recurrence. Infiltrated GBM cells are difficult to completely eradicate surgically and with local therapeutic modalities. Although much effort has focused on understanding the various mechanisms controlling GBM invasiveness, the nature of the invasiveness remains poorly characterized. Here, we established a highly invasive glioma cell line (U87R4 cells) and a non-invasive cell line (U87L4 cells) from U87MG glioma cells following four rounds of serial in vivo intracranial transplantation. Compared to U87L4 cells, U87R4 cells were highly invasive and had glioma stem cell-like properties. Microarray analysis showed that apoptosis-inducing genes (caspase3 and PDCD4) were downregulated, whereas several cancer stem cell-relevant genes (Wnt10A, Frizzled 4, and CD44) were upregulated in U87R4 cells compared to U87L4 cells. U87R4 cells were resistant to anticancer drug-induced cell death, which was partially due to downregulation of caspase3 and PDCD4. U87R4 cells retained activated Wnt/β-catenin signaling through Frizzled 4, which was sufficient to control neurosphere formation. In addition, Frizzled 4 promoted expression of the epithelial to mesenchymal transition regulator, SNAI1, and acquisition of a mesenchymal phenotype. Taken together, our results indicate that Frizzled 4 may be a member of the Wnt signaling family that governs both stemness and invasiveness of glioma stem cells, and may be a major cause of GBM recurrence and poor prognosis. We established a highly invasive glioma cell line (U87R4 cells) and a non-invasive cell line (U87L4 cells) from U87MG glioma cells following four rounds of serial in vivo intracranial transplantation to characterize the mRNA expression profile of highly invasive glioma cells compared to non-invasive/parental glioma cell lines.
2010-05-27 | E-GEOD-21570 | biostudies-arrayexpress