Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Control of brain tumor growth by reactivating monocytes and macrophages with niacin

ABSTRACT: We have found that innate immune cells (monocytes/macrophages) are compromised in malignant glioma, and we have determined that vitamin B3 (niacin) reactivates and/or reprograms monocytes/macrophages to inhibit glioma growth, particularly by suppressing the growth of brain tumor initiating cells (BTICs). To this end, we sought to obtain insights into the mechanisms by which niacin regulates monocyte/macrophage activity to alter glioma growth. Analysis of the microarray data identified several genes that were differentially altered in niacin-treated monocytes that could regulate BTIC growth. The study has identified a mechanistic basis for the regulation of glioma growth with niacin treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE103381 | GEO | 2017/09/05

SECONDARY ACCESSION(S): PRJNA401840

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

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.

2016-05-18 | E-GEOD-81515 | biostudies-arrayexpress

Effect of demeclocycline on brain tumor initiating cells

2016-05-18 | GSE81515 | GEO

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.

2016-05-01 | GSE79735 | 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

Candida glabrata transcription profile when grown under Niacin starvation or in human urine

Project description:The transcription profile of Candida glabrata grown under two different Niacin limitation conditions were determined. Condition 1 is comparing log phase C. glabrata cells (O.D. 0.5-0.6) grown in synthetic medium containing 0.016 uM versus 3.25 uM nicotinic acid (NA), a common form of Niacin. The NA concentration of 3.25 uM is the standard concentration in synthetic complete (SC) medium. Condition 2 is comparing log phase C. glabrata cells (O.D. 0.4-0.6) grown in 3 individual human urine samples (supplemented with 2% glucose) versus in SC medium. Keywords: transcriptional profiling by microarray GSM151863, GSM151869 are dye-swap experiment #1 and GSM151880, GSM151881 are dye-swap experiment #2 for Niacin limitation condition 1. GSM151934, GSM152116 are dye-swap experiment #1, GSM152118, GSM152119 are dye-swap experiment #2 and GSM152130, GSM152131 are dye-swap experiment #3 for Niacin limitation condition 2.

2010-06-05 | E-GEOD-6582 | biostudies-arrayexpress

Diabetic mice fat- niacin bound chromium

Project description:To study effect of niacin bound chromium in changing genetic profile of subcutaneous fat from diabetic mice Keywords: nutritional supplemetation, obesity

2007-03-05 | GSE4420 | GEO

PD-1 independent of PD-L1 promotes glioblastoma growth through the NF B pathway

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

Gene expression profiles of Sunitinib-treated but not untreated short-term serum-free cultures predict treatment response of human high-grade gliomas in vitro

Project description:High-grade gliomas are amongst the most deadly human tumors. Treatment results are overall disappointing. Nevertheless, in several trials around 20% of patients respond to therapy. Diagnostic strategies to identify those patients that will ultimately profit from a specific targeted therapy are urgently needed. Gene expression profiling of untreated tumors is a well established approach for identifying biomarkers or diagnostic signatures. However, reliable signatures predicting treatment response in gliomas do not exist. Here we suggest a novel strategy for developing diagnostic signatures. We postulate that predictive gene expression patterns emerge only after tumor cells have been treated with the agent in vitro. Moreover, we postulate that enriching specimens for tumor initiating cells sharpens predictive expression patterns. Here, we report on the prediction of treatment response of cancer cells in vitro. As a proof of principle we analyzed gene expression in 18 short-term serum-free cultures of high-grade gliomas enhanced for brain tumor initiating cells (BTIC) before and after in vitro treatment with the tyrosine kinase inhibitor Sunitinib. Profiles from treated but not from untreated glioma cells allowed to predict therapy-induced impairment of proliferation of glioma cells in vitro. Prediction can be achieved with as little as 6 genes allowing for a straightforward translation into the clinic once the predictive power of the signature is shown also in vivo. Our strategy of using expression profiles from in vitro treated BTIC-enriched cultures opens new ways for trial design for patients with malignant gliomas. 72 samples; 18 brain tumor initiating cells (BTICs); 4 treatment conditions: 1 ÂµM Sunitinib or 0.00025% DMSO with and without the combination of recombinant growth factors VEGF and PDGF-AB for 6 hours

2014-10-07 | E-GEOD-51305 | biostudies-arrayexpress

Transcription profiling of subcutaneous fat from mice supplemented with niacin bound chromium or water for ten weeks to study effect of niacin bound chromium on genetic profile in diabetic mice.

Project description:To study effect of niacin bound chromium in changing genetic profile of subcutaneous fat from diabetic mice Experiment Overall Design: Two groups (n=4 each group) of mice were supplemented (oral gavage) with: i) niacin bound chromium (10 mg/kg body wt) in water for 10 wks (5d/wk) or ii) matching volume of water. After 10 wks of supplementation the subcutaneous fat was harvested and gene expression profile was studied using Affymetrix mouse genome 430 v 2.0 chips.

2007-11-22 | E-GEOD-4420 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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