Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

35 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Glioblastoma-initiating cells from the peritumoral tissue have an invasive phenotype that is dependent on Rac and RhoA activation and downregulation of cytoplasmic p27.

ABSTRACT: The invasive nature of glioblastoma (GBM) represents a major clinical challenge contributing to poor outcomes. Invasion of GBM into healthy tissue restricts therapeutic access and surgical resection. Therefore, effective anti-invasive strategies of GBM cells can be key to increase the efficacy of chemotherapy against this devastating disease. As cancer stem or initiating cells are considered to retain the tumorigenic potential in a number of tumors including glioblastoma, we studied the invasion capabilities of glioblastoma initiating cells (GICs) that were isolated from the peritumoral (PT) tissue, which surrounds the tumor mass (TM) and remains in the brain after tumor removal. We found that PT-GICs are less proliferative but more invasive compared to TM-GICs. Gene expression arrays of cells derived from the tumor mass and the peritumoral tissue of three glioblastoma cases

ORGANISM(S): Homo sapiens

SUBMITTER: Victor Segura

PROVIDER: E-GEOD-37985 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Glioblastoma-initiating cells from the peritumoral tissue have an invasive phenotype that is dependent on Rac and RhoA activation and downregulation of cytoplasmic p27.

Project description:The invasive nature of glioblastoma (GBM) represents a major clinical challenge contributing to poor outcomes. Invasion of GBM into healthy tissue restricts therapeutic access and surgical resection. Therefore, effective anti-invasive strategies of GBM cells can be key to increase the efficacy of chemotherapy against this devastating disease. As cancer stem or initiating cells are considered to retain the tumorigenic potential in a number of tumors including glioblastoma, we studied the invasion capabilities of glioblastoma initiating cells (GICs) that were isolated from the peritumoral (PT) tissue, which surrounds the tumor mass (TM) and remains in the brain after tumor removal. We found that PT-GICs are less proliferative but more invasive compared to TM-GICs.

2015-05-13 | GSE37985 | GEO

Expression profiles of microRNAs in Glioma-Initiating Cells (GICs) cultured under hypoxia and normoxia

2015-12-28 | GSE73625 | GEO

Expression data for KDM1B knockdown in Glioma-Initiating Cells (GICs)

Project description:Glioblastoma (GBM) is the most common and aggressive primary brain tumor in adults, with glioma initiating cells (GICs) implicated to be critical for tumor progression and resistance to therapy. KDM1B is involved in regulating GICs' responses to hypoxia, since over-expression of KDM1B delays the cell growth under hypoxia while knocking-down of KDM1B in GICs promotes their survival and tumorigenic abilities.

2015-12-28 | GSE73573 | GEO

GPR56/ADGRG1 inhibits Mesenchymal Differentiation and Radioresistance in Glioblastoma [GIC7]

Project description:A mesenchymal transition occurs both during natural evolution of glioblastoma (GBM) and in response to therapy. However, the molecular mechanisms underlying mesenchymal differentiation are not well understood. We have found that the adhesion G protein-coupled receptor GPR56/ADGRG1 inhibits mesenchymal differentiation and radioresistance in glioblastoma stem-like initiating cells (GICs). Here, we have performed microarray analysis of parental- versus GPR56 knockout-GICs to identify gene expression changes upon GPR56 knockout

2017-10-31 | GSE104653 | GEO

Expression data from Glioma-Initiating Cells (GICs) cultured under hypoxia and normoxia

Project description:Glioblastoma (GBM) is the most common and aggressive primary brain tumor in adults, with glioma initiating cells (GICs) implicated to be critical for tumor progression and resistance to therapy. The hypoxic tumor microenvironment has been shown to play an important role to maintain the GICs; however, the mechanisms regulating responses of GICs to hypoxia remain poorly understood. We used microarray to to detail the global change of gene expression in GICs cultured under hypoxia compared to normoxia and identified de-regulated genes during hypoxia. CD133+ D456MG GICs were cultured under 1% O2 or 20% O2 for 12 hours. Then RNA was extracted and gene expression was profiled by microarray.

2016-07-03 | E-GEOD-73556 | biostudies-arrayexpress

Expression data from Glioma-Initiating Cells (GICs) cultured under hypoxia and normoxia

Project description:Glioblastoma (GBM) is the most common and aggressive primary brain tumor in adults, with glioma initiating cells (GICs) implicated to be critical for tumor progression and resistance to therapy. The hypoxic tumor microenvironment has been shown to play an important role to maintain the GICs; however, the mechanisms regulating responses of GICs to hypoxia remain poorly understood. We used microarray to to detail the global change of gene expression in GICs cultured under hypoxia compared to normoxia and identified de-regulated genes during hypoxia.

2016-01-01 | GSE73556 | GEO

GPR56/ADGRG1 inhibits Mesenchymal Differentiation and Radioresistance in Glioblastoma

Project description:A mesenchymal transition occurs both during natural evolution of glioblastoma (GBM) and in response to therapy. However, the molecular mechanisms underlying mesenchymal differentiation are not well understood. We have found that the adhesion G protein-coupled receptor, GPR56/ADGRG1, inhibits mesenchymal differentiation and radioresistance in glioblastoma stem-like initiating cells (GICs). Here, we have performed microarray analysis of control- versus GPR56 knockdown-GICs to characterize gene expression changes upon GPR56 knockdown and identify a gene expression signature associated to GPR56.

2017-10-01 | GSE94765 | GEO

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

Analysis of microRNA expression profile in malignant glioma tissues

Project description:Malignant gliomas represent the most devastating group of brain tumors in adults, among which glioblastoma multiforme (GBM) exhibits the highest malignancy rate. Despite combined modality treatment, GBM recurs and is invariably fatal. A further insight into molecular background of gliomagenesis is required to improve patient outcome. The first aim of this study was to gain broad information on miRNA expression pattern in malignant gliomas, mainly GBM. We investigated the global miRNA profile of malignant glioma tissues by means of miRNA microarrays, deep sequencing and meta-analysis. We selected miRNAs the most frequently deregulated in glioblastoma tissues as well as peritumoral brain areas in comparison to normal human brain. We found candidate miRNAs contributing to progression from gliomas grade III to gliomas grade IV. The meta-analysis of miRNA profiling studies in GBM tissues summarizes the past and recent advances in an investigation of miRNA signature in GBM versus noncancerous human brain and provides a comprehensive overview. We proposed a set of 35 miRNAs which expression is the most frequently deregulated in GBM patients and 30 miRNA candidates recognized as novel GBM biomarkers. miRNA expression profile in the adult malignant gliomas, glioma peritumoral tissues and normal human brain.

2014-09-26 | E-GEOD-61710 | biostudies-arrayexpress

Microarray to study the effects of Snail overexpression in Glioblastoma cells.

Project description:Snail1 is a transcription factor known to promote the epithelial to mesenchymal transition process and stemness. We have previously described that in Glioblastoma BMP7 promotes glioblastoma initiating cells (GICs) to differentiate towards the astrocytic lineage and to lose their self-renewal capacity in a Snail-dependent manner. In order to elucidate how Snail promotes GIC differentiation, we decided to stably overexpress Snail in the U2987 glioblastoma cells. To understand which genes are regulated by Snail we performed a microarray screen with the Affymetrix U133plus2 platform and total RNA from U2987MG cells stably expressing Snail (U2987MG-Snail cells; clones F and G) versus control cells (clones A and B), two biological replicates per condition.

2018-01-15 | E-MTAB-6151 | 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