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Brain tumor initiating cell response to microglia

ABSTRACT: Determination of the mechanism by which microglia regulate growth of brain tumor initiating cells (BTICs) and differentiation. Results identify the factors involved in the regulation and provide mechanistic basis. We subjected brain tumor initiating cells to microarray to determine the genes involved in BTICs growth and differentiation when exposed to microglia conditioned medium (MCM) for 6h.

ORGANISM(S): Homo sapiens

PROVIDER: GSE52127 | GEO | 2013/11/06

SECONDARY ACCESSION(S): PRJNA226782

REPOSITORIES: GEO

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Brain tumor initiating cell response to microglia

Project description:Determination of the mechanism by which microglia regulate growth of brain tumor initiating cells (BTICs) and differentiation. Results identify the factors involved in the regulation and provide mechanistic basis. We subjected brain tumor initiating cells to microarray to determine the genes involved in BTICs growth and differentiation when exposed to microglia conditioned medium (MCM) for 6h. BTICs were grown in MCM or control medium for 6h, and media was removed and then the cells were subjected for RNA extraction and hybridization on Affymatrix microarrays. Three (3) control and four (4) MCM samples were generated. The overall objective was to collect the RNA from the MCM exposed differentiated BTICs.

2013-11-06 | E-GEOD-52127 | biostudies-arrayexpress

Effect of demeclocycline on brain tumor initiating cells

Project description:We have determined that demeclocycline reduces the growth of brain tumor initiating cells (BTICs). Specifically, we sought to obtain insights into the mechanisms by which demeclocycline directly regulates BTIC growth. Analysis of the array data identified several genes that were altered with demeclocycline treatment that could regulate BTIC growth. The study provides the mechanistic basis for the regulation of BTIC growth with demeclocycline treatment. We subjected 3 BTIC lines to microarray analyses to identify genes involved in the regulation of BTIC growth by demeclocycline. Three BTIC lines (BT012, BT025 and BT048) were treated with 10 ÂµM demeclocycline for 6h. One (1) control and 1 treatment (demeclocycline treated) sample was generated from each BTIC line. Thus, a total of 6 RNA samples from 3 BTIC lines were obtained for microarray analysis.

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Effect of demeclocycline on brain tumor initiating cells

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Effect of tenascin C on brain tumor initiating cells

Project description:We have determined that tenascin C (TNC) regulates the growth of human brain tumor initiating cells (BTICs). We have identified novel mechanisms by which TNC regulates BTIC growth. Analysis of the array data identified a number of genes that were altered with TNC treatment that could potentially regulate BTIC growth. The study provides the mechanistic basis for the regulation of BTIC growth with TNC.

2017-02-08 | GSE94640 | GEO

RNA-seq Profiles in RBPJ Maintains Brain Tumor Initiating Cells through CDK9-mediated Transcriptional Elongation

Project description:Glioblastomas coopt stem cell regulatory pathways to maintain brain tumor initiating cells (BTICs), also known as cancer stem cells. Notch signaling has been a molecular target in BTICs, but Notch antagonists have demonstrated limited efficacy in clinical trials. RBPJ is considered a central transcriptional mediator of Notch activity. Here, we report that pharmacologic Notch inhibitors were less effective than targeting RBPJ in suppressing tumor growth. While Notch inhibitors decreased canonical Notch gene expression, RBPJ regulated a distinct profile of genes critical to BTIC stemness and cell cycle progression. RBPJ was preferentially expressed by BTICs and required for BTIC self-renewal and tumor growth. MYC, a key BTIC regulator, bound the RBPJ promoter and treatment with a BET family bromodomain inhibitor decreased MYC and RBPJ expression. Proteomic studies demonstrated that RBPJ binds CDK9, a component of P-TEFb (positive transcription elongation factor), to target gene promoters, enhancing transcriptional elongation. Collectively, RBPJ links MYC and transcriptional control through CDK9, providing potential nodes of fragility for therapeutic intervention, potentially distinct from Notch.

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GTP Cyclohydrolase I Confers Metabolic Protection Against Lipid Peroxidation in Glioblastoma

Project description:Guanosine triphosphate cyclohydrolase I (GCH1) was previously identified as a regulator of reactive oxygen species (ROS) in brain tumor initiating cells (BTICs). Elucidating the GCH1/Tetrahydrobiopterin (BH4) pathway in BTICs has unveiled the necessity for GCH1 to protect BTICs from lipid peroxidation. Within this study, we observed differences in lipid pathways and lipid metabolites during GCH1 modulation. Alteration to polyunsaturated fatty acids (PUFAs), a species of oxidatively vulnerable lipids, were altered during GCH1 knockdown. Pharmacological inhibition of BH4 with drugs known to cross the blood brain barrier (sulfasalazine and pyrimethamine) successfully reduced growth in GCH1 overexpressed BTICs, induced lipid peroxidation.

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Gene Expression Profile of ING5-knockdown Brain Tumor Initiating Cell Lines

Project description:Transcriptome analysis on ING5-knockdown brain tumor stem cell lines Stem cell-like brain tumor initiating cells (BTICs) cause recurrence of glioblastomas, with BTIC "stemness" affected by epigenetic mechanisms. The ING family of epigenetic regulators (ING1-5) function by targeting histone acetyltransferase (HAT) or histone deacetylase (HDAC) complexes to the H3K4me3 mark to alter histone acetylation and subsequently, gene expression. Here we find that ectopic expression of ING5, the targeting subunit of HBO1, MOZ and MORF HAT complexes increases expression of the Oct4, Olig2 and Nestin stem cell markers, promotes self-renewal, prevents lineage differentiation and increases stem cell pools in BTIC populations. This activity requires the plant homeodomain region of ING5 that interacts specifically with the H3K4me3 mark. ING5 also enhances PI3K/AKT and MEK/ERK activity to sustain self-renewal of BTICs over serial passage of stem cell-like spheres. ING5 exerts these effects by activating transcription of calcium channel and follicle stimulating hormone (FSH) pathway genes. In silico analyses of The Cancer Genome Atlas (TCGA) data suggest that ING5 is a positive regulator of BTIC stemness, whose expression negatively correlates with patient prognosis, especially in the Proneural and Classical subtypes, and in tumors with low SOX2 expression. These data suggest that altering histone acetylation status and signaling pathways induced by ING5 may provide useful clinical strategies to target tumor resistance and recurrence in glioblastoma.

2017-06-24 | GSE100398 | GEO

H3K27ac ChIP-seq BTIC vs. DGC

Project description:Brain tumor initiating cells (BTICs), also known as cancer stem cells, hijack high-affinity glucose uptake normally active in brain to maintain energy demands in dynamic tumor microenvironments. Using unbiased metabolomics and genomic analyses, we discovered that de novo purine synthesis is functionally upregulated in BTICs, mediating glucose-sustained anabolic metabolism. Inhibiting purine synthesis abrogated BTIC growth, self-renewal, and in vivo tumor formation by depleting intracellular pools of purine nucleotides, supporting purine synthesis as potential therapeutic point of fragility. In contrast, differentiated brain tumor cells retained proliferative potential with targeting of purine biosynthetic enzymes, suggesting a selective dependence in BTICs. Upstream transcriptional activation of purine synthesis is mediated by MYC. Elevated expression of purine synthetic enzymes correlates with poor prognosis in glioblastoma patients. Collectively, our results suggest that a stem-like state in brain cancer is associated with metabolic reprogramming to fuel tumor hierarchy, revealing potential BTIC cancer dependencies amenable to targeted therapy.

2017-03-20 | GSE95216 | GEO

Disulfiram when combined with copper enhances the therapeutic effects of temozolomide for the treatment of Glioblastoma

Project description:Dilsulfiram together with Copper shows efficacy against patient derived Brain Tumor Initiating Cells (BTICs) in vitro and sensitizes BTICs to the DNA damaging agent TMZ. In addition, preclinical assessment found that DSF/Cu potentiaties the efficicacy of TMZ in vivo and prolongs survival. We used microarrays to detail the global profile of gene expression underlying DSF/Cu treatment in vitro and in vivo in BTICs.

2016-03-21 | GSE76146 | GEO

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Project description:we found that a proportion of human and murine brain tumor-initiating cells (BTICs) expressed programmed cell death protein (PD-1) in situ and in culture. PD-1 signaling through NF B promotes BTIC proliferation.

2020-10-30 | GSE160417 | GEO

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