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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression profiling of sox11-expressing glioma-initiating cell-like cells

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Toru Kondo

PROVIDER: E-GEOD-17076 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Sox11 prevents tumorigenesis of glioma-initiating cells by inducing neuronal differentiation.

Hide Takuichiro T Takezaki Tatsuya T Nakatani Yuka Y Nakamura Hideo H Kuratsu Jun-ichi J Kondo Toru T

Cancer research 20091006 20

Recent findings have shown that malignant tumors contain cancer-initiating cells (CIC), which self-renew and are tumorigenic. However, CICs have not been characterized properly due to lack of specific markers. We recently established a mouse glioma cell line, NSCL61, by overexpressing an oncogenic HRas(L61) in p53-deficient neural stem cells. Using limiting dilution assays, we show that only 2 of 24 NSCL61 clones retained their tumorigenicity in vivo, although the others also expressed oncogenic ...[more]

PMID: 19808959

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Expression profiling of sox11-expressing glioma-initiating cell-like cells

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.

2009-12-01 | GSE17076 | GEO

Expression profiling of mouse glioma-initiating cell-like cells (GICs) and non-GICs

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Expression profiles of mouse glioma-initiating cells.

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Expression data from glioma cells exposed to interferon (IFN)-beta

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2014-03-31 | E-GEOD-53213 | biostudies-arrayexpress

Chromatin remodeling factor BRG1 regulates stemness and chemosensitivity of glioma initiating cells

Project description:Glioblastoma multiforme (GBM) is a highly aggressive and malignant brain tumor that is refractory to existing therapeutic regimens due in part to the presence of stem-like cells, termed Glioma-Initiating Cells (GICs). The complex interactions between different signaling pathways and epigenetic regulation of key genes may be critical in the maintaining GICs in their stem-like state. Although several signaling pathways have been identified as being dysregulated in GBM, the prognosis of GBM patients remains miserable despite improvements in targeted therapies. In this report we identified that the BRG1 catalytic subunit of the SWI/SNF chromatin remodeling complex plays a fundamental role in the maintaining GICs in their stem-like state. In addition, we identified a novel mechanism by which BRG1 maintains glucose levels critical for GICs. BRG1 downregulates the expression of TXNIP, a negative regulator of glycolysis. BRG1 knockdown led to STAT3 upregulation, which in turn led to TXNIP activation. We further identified that TXNIP is a STAT3-regulated gene. Moreover, BRG1 suppressed the expression of interferon-stimulated genes, which regulate tumorigenesis. We also demonstrate that BRG1 plays a critical role in the drug resistance of GICs and in GIC-induced tumorigenesis. By genetic and pharmacological means, we found that inhibition of BRG1 can sensitize GICs to chemotherapeutic drugs, temozolomide and Carmustine. Our studies suggest that BRG1 may be a novel therapeutic target in GBM. The identification of the critical role that BRG1 plays GIC stemness and chemosensitivity in GICs will inform the development of better targeted therapies in GBM and possibly other cancers.

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