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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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE37985 | GEO | 2015/05/13

SECONDARY ACCESSION(S): PRJNA166873

REPOSITORIES: GEO

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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. Gene expression arrays of cells derived from the tumor mass and the peritumoral tissue of three glioblastoma cases

2015-05-13 | E-GEOD-37985 | biostudies-arrayexpress

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

Identification of novel genes associated with human glioblastoma (GBM) tumor-initiating cells (TICs)

Project description:Most patients affected by Glioblastoma multiforme (GBM) experience a recurrence of the disease because of the spreading of tumor-initiating cells (TICs) beyond surgical boundary. Unveiling and targeting molecular mechanisms causing this process is a logic goal to impair GBM killing ability. In an orthotopic xenograph model, we have noticed that GBM TICs isolated from several patients may fall into two classes of invasive behavior: nodular or diffuse. In order to identify genes responsible for the diffusive type of invasion, we have compared by genome expression analysis, cultured GBM TICs belonging to the two classes. This analysis allowed us to identify a small group of regulated genes in the diffusive type of GBM TICs. The gene ontology process of cell adhesion and the localization of the gene product functions to the plasmamembrane resulted significantly associated to this gene set. Real time RT-PCR and immunofluorescence analyses performed for a selected subgroup of regulated genes/gene products confirmed the results obtained by the expression analysis. Some of the genes that we found upregulated in our screening were already proven to be involved in Glioma cell invasion supporting our study. However, we have also identified genes that were not previously implicated in this process. To assess whether these are required to sustain TICs GBM invasion, we silenced a subset of them and evaluated in Boyden chamber the invasive ability of the cells. Our study provides novel target genes to be evaluated for the inhibition of GBM diffusion within the SNC. As we observed that GBM TICs may fall into two classes of M-bM-^@M-^\in vivoM-bM-^@M-^] invasive behavior in mouse orthotopic transplantation: expansive or highly diffusive, resulting in the hostM-bM-^@M-^Ys white and gray matters substitution, we decided to identify genes associated with the latter phenotype by microarray analysis. Three replicates of each class were analyzed.

2012-09-11 | E-GEOD-16805 | 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

AN1 type zinc finger protein 3 ZFAND3 is part of a transcriptional complex that drives Glioblastoma invasion

Project description:The infiltrative nature of Glioblastoma (GBM), the most aggressive primary brain tumor, critically prevents complete surgical resection and masks tumor cells behind the blood brain barrier reducing the efficacy of systemic treatment. New insight in molecular pathways underlying invasion to identify novel invasion-specific molecular targets are likely to improve treatment success and patient outcome. In the present study, we used a genome-wide interference screen to determine invasion-essential genes and identified the AN1/A20 zing finger domain containing protein 3 (ZFAND3) as a crucial driver of invasion in GBM. Using patient-derived cellular GBM models, we validated that loss of ZFAND3 dampens the invasive capacity of GBM, whereas ZFAND3 overexpression increases motility in GBM cells that were initially not invasive. At the mechanistic level, we demonstrate that ZFAND3 activity requires nuclear localization and integral zinc-finger domains. Using integrated transcriptomic and proteomic approaches coupled with reporter assays, we identify ZFAND3 as a novel functional member of a protein complex encompassing PUF60 to activate transcription and GBM cell invasion. Our findings indicate that ZFAND3 regulates the promoter of invasion-related genes such as COL6, FN1 and NRCAM through direct binding to GC rich regions. To harness the therapeutic potential of this transcriptional complex, further investigation in ZFAND3 function in GBM and related invasive cancer types is warranted.

2020-10-08 | MSV000086247 | MassIVE

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