Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

46 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Publications

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

Similar Datasets

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

Project description:To identify factors involved in glioma-initiating cells (GICs), we compared gene expression between GIC-like cells and non-GICs. Neural stem cells (NSCs) were transfected with pCMS-EGFP-HRasL61 and pBabe-neo by electroporation and cultured in 0.5 mg/ml neomycin. The GFP-positive stable NSCs (NSCL61s) were purified by flow cytometry. Total RNA was prepared using RNeasy Mini Kit (QIAGEN).

2009-11-30 | E-GEOD-17062 | biostudies-arrayexpress

Expression profiles of mouse glioma-initiating cells.

Project description:To identify factors involved in glioma-initiating cells (GICs), we compared gene expressions between GIC-like cells and non-GICs. p53-deficient Neural stem cells (NSCs), oligodendrocyte precursor cells (OPCs), and astrocytes (ASTs) were transfected with pCMS-EGFP-HRasL61 and pBabe-neo by electroporation and cultured in 0.5 mg/ml neomycin. The GFP-positive stable NSCs (NSCL61s), OPCs (OPCL61s) and ASTs (ASTL61s) were purified by flow cytometry. Total RNA was prepared using a RNeasy Mini Kit (QIAGEN) and used for the expression analysis.

2011-06-01 | E-GEOD-28091 | biostudies-arrayexpress

Expression profiles of mouse glioma-initiating cells.

Project description:To identify factors involved in glioma-initiating cells (GICs), we compared gene expressions between GIC-like cells and non-GICs.

2011-06-01 | GSE28091 | GEO

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

Project description:To identify factors involved in glioma-initiating cells (GICs), we compared gene expression between GIC-like cells and non-GICs.

2009-12-01 | GSE17062 | GEO

Expression profiling of glioma initiating cells (GICs) in the sphere and differentiation conditions

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. Within 4 hours of tumor removal from GBM patients, tissues were subjected to GIC preparation. After successive cloning, total RNA from GIC clones (GIC03A and GIC03U) on day 2 or 7 of subculture in NSC medium with or without 10% FCS was subjected to the analysis with Affymetrix microarrays. Simultaneously, the proteins extracted from the same set of cells were subjected to LC-shot gun analyses using the 8-plex iTRAQ method. We sought to obtain the information of the common molecules that were up- or down-regulated during the GSC differentiation process, and functional targets for the early onset of GIC-associated glioma.

2013-01-26 | E-GEOD-43762 | biostudies-arrayexpress

Expression profiling of glioma initiating cells (GICs) in the sphere and differentiation conditions

2013-01-26 | GSE43762 | GEO

Development of microRNA (miRNA) expression signatures for mouse glioma-initiating cells (GICs)

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

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.

2018-07-03 | GSE116545 | GEO

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

Project description:Glioma cells are sensitized to the alkylator temozolomide after exposure to IFN-beta. In glioma-initiating cells (GIC), IFN-beta alone reduces clonogenicity. We investigated differentially expressed genes with or without IFN exposure in either longterm glioma cells or GIC. We used microarrays to investigate differential gene regulation in glioma cells after exposure to either ddH20 or IFN-beta 300 IU/ml at 6 h or 24 h. We used either the longterm cell line LNT-229 or the GIC cell lines GS-2 and GS-9 and exposed them to either IFN-beta 300 IU/ml or ddH20 for 6 h or 24 h.

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data