GEO DataSets

(Submitter supplied) We described the metabolic alterations in glioblastoma model systems elicited by AURKA inhibition. By utilizing proteomic and transcriptomic analyses coupled with untargeted polar and nonpolar metabolite analysis by LC/MC, we found that AURKA inhibition leads to a profound reprogramming of tumor metabolism, which suppresses c-Myc protein levels and increases pro-survival PGC1α which in concert mediate a suppression of glycolysis and a concomitant activation of oxidative phosphorylation (OXPHOS) that is fueled by enhanced fatty acid oxidation (FAO). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17930

4 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

6 Samples

Download data: BIGWIG

(Submitter supplied) By integration of transcriptome, CHIP-seq, ATAC-seq, proteomic and metabolite screening followed by carbon tracing (U-13C-Glucose, U-13C-Glutamine and U-13C-Palmitic acid) and extracellular flux analysis we provided evidence that genetic (shRNA and CRISPR/Cas9) and pharmacological (Alisertib) AURKA inhibition elicited substantial metabolic reprogramming supported in part by inhibition of MYC targets and concomitant activation of PPARA signaling. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

2 Samples

Download data: BIGWIG

(Submitter supplied) By integration of transcriptome, CHIP-seq, ATAC-seq, proteomic and metabolite screening followed by carbon tracing (U-13C-Glucose, U-13C-Glutamine and U-13C-Palmitic acid) and extracellular flux analysis we provided evidence that genetic (shRNA and CRISPR/Cas9) and pharmacological (Alisertib) AURKA inhibition elicited substantial metabolic reprogramming supported in part by inhibition of MYC targets and concomitant activation of PPARA signaling. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

4 Samples

Download data: BIGWIG

(Submitter supplied) By utilizing proteomic and transcriptomic analysis coupled with untargeted polar and non-polar metabolite analysis by liquid chromatography/mass spectrometry, we identified a specific metabolic program elicited by c-MET inhibition. Interference with c-MET drives oxidative metabolism by increasing fatty acid oxidation (FAO) and glucose anaplerosis, which was orchestrated by the master-regulator, PGC1α. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL26944

4 Samples

Download data: CEL

(Submitter supplied) Gene expression of chronically or acutely Crizotinib treated glioblastoma cells vs vehicle controls

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17930

4 Samples

Download data: CEL

(Submitter supplied) FDA-approved global (panobinostat, vorinostat) and selective (romidepsin) histone-deacetylase (HDAC) inhibitors elicit metabolic reprogramming in concert with disruption of several Warburg-effect related super-enhancers

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL11154

8 Samples

Download data: BIGWIG

(Submitter supplied) Inhibition of BRD proteins by OTX015, and inhibition of HDAC by Panobinostat and the combination alters the gene expression of the glioblastoma cells. To compare the drug effect and find out the resonal of the synergisty of the bombination, we performed microarray experiments.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17930

8 Samples

Download data: CEL

(Submitter supplied) Panobinostat is a non-selective histone deactylase inhibitor which has been approved by FDA for treatment of mutiple myeloma. Whether and how the drug works on glioblastoma remains unclear. Here we treated mice implanted with patient derived xenograft glioblastoma G43 with DMSO or Panobinostat and harvest the tumors for microarray analysis for gene expression results.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17930

2 Samples

Download data: CEL

(Submitter supplied) Low dose of HDAC inhibitor (Panobinostat) treatment causes U87 cells to become resistant to the drug. Gene expression of the resistant cell line is altered comparing to the vehicle control.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17930

2 Samples

Download data: CEL

(Submitter supplied) Glioblastoma (GBM) is among the most aggressive of human cancers. Although differentiation therapy has been proposed to be potential approach to treat GBM, the mechanisms of induced differentiation remain poorly defined. Here, we established the induced differentiation model of GBM by using cAMP activators, which specifically directed GBM into astroglia. Next, transcriptomic and proteomic analyses uncovered oxidative phosphorylation and mitochondrial biogenesis were involved in induced differentiation of GBM. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

5 Samples

Download data: TXT

(Submitter supplied) We performed microarray analysis in order to evaluate the effect of ONC201 and its derivatives (ONC206 and ONC212) on gene expression in U87 glioma cells.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17930

4 Samples

Download data: CEL

(Submitter supplied) We performed microarray analysis in order to evaluate the effect of ONC201 on gene expression in glioma cells (U87).

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17930

2 Samples

Download data: CEL

(Submitter supplied) To identify ceRNA network associated with GBM, a hybridization-based microarray assay was used to analyze three paired GBM tissues with lower expression of miR-422a.

Organism:

Homo sapiens

Type:

Non-coding RNA profiling by array

Platform:

GPL22120

6 Samples

Download data: TXT

(Submitter supplied) We investigate the role of lactic acid in GBM cells as an epigenetic metabolite in the regulation of pro-survival gene expression.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL27949

12 Samples

Download data: CEL

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL570 GPL9115

13 Samples

Download data: BED, CEL

(Submitter supplied) EGFRvIII is the most common deletion mutant of EGFR in human cancer and its levels are highly correlated with poor prognosis in GBM. The deletion of exons 2-7 removes most of the extracellular ligand binding domain, so it is unable to bind EGF or other EGFR-binding ligands. Nevertheless, the mutant receptor is constitutively phosphorylated, and is capable of activating downstream signaling pathways at a low level. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

8 Samples

Download data: CEL

(Submitter supplied) We present a computational method for building a regulatory network from global phosphoproteomic and transcription profiling data. To recover the critical missing links between signaling events and transcriptional responses, we relate changes in chromatin accessibility to changes in expression and then uses these links to connect proteomic and transcriptome data. We applied our approach to integrate epigenomic, phosphoproteomic and transcriptome changes induced by the variant III mutation of the epidermal growth factor receptor (EGFRvIII) in a cell line model of glioblastoma multiforme (GBM).

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL9115

5 Samples

Download data: BED