GEO DataSets

(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) 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) 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) 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) 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) Pan and selective HDAC inhibition is synthetically lethal with TRAP1 inhibition in various model systems of glioblastoma, including patient derived xenograft (PDX) cells. Mechanistically, this occurs through several mechanisms, including the induction of metabolic stress by interference with tumor cell energy metabolism accompanied by modulation of pro- and anti-apoptotic Bcl-2 family proteins and the induction of a cell death with apoptotic features.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL20301

2 Samples

Download data: BIGWIG

(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) By integration of transcriptome and metabolite analyses, we showed that pharmacological activation of the mitochondrial ClpP protease through utilization of enhanced imipridone compounds (ONC206 and ONC212) in combination with global (Panobinostat) and selective (romidepsin) HDAC – inhibitors caused synergistic reduction of viability in established and patient-derived xenograft (PDX) cultures of human GBM. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL27949

8 Samples

Download data: CEL

(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) comparative genome hybridisation of Hdac1/2 cKO lymphomas and matched normal tissue Histone deacetylases (HDACs) are epigenetic erasers of lysine-acetyl marks. Inhibition of HDACs using small molecule inhibitors (HDACi) is a potential strategy in the treatment of various diseases and is approved for treating hematological malignancies. Harnessing the therapeutic potential of HDACi requires knowledge of HDAC-function in vivo. more...

Organism:

Mus musculus

Type:

Genome variation profiling by genome tiling array

Platform:

GPL13924

6 Samples

Download data: PAIR, TXT

(Submitter supplied) Determine the differences in gene expression profiles of MV-4-11 AML cells treated with HDAC1/2-selective inhibition, azacitidine, or the combination of the two agents. Acute myeloid leukemia (AML) is a heterogeneous group of hematopoietic stem cell disorders characterized by defects in myeloid differentiation and increased proliferation of neoplastic hematopoietic precursor cells. Outcomes for patients with AML remain poor, highlighting the need for novel treatment options. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL15207

4 Samples

Download data: CEL

(Submitter supplied) Glomerular diseases are most common cause of end stage kidney disease (ESKD). Although renin angiotensin system inhibitors are effective for progression of chronic kidney disease, The number of ESKD increases in the world. To identify a new candidate drug for glomerular disease, differentially expressed genes are searched by glomerular RNA microarray.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL16570

8 Samples

Download data: CEL, CHP

(Submitter supplied) Gene expression data from BE(2)-C cells treated in triplicate with either vehicle (DMSO), 5 μM all-trans retinoic acid (ATRA), 1 mM valproic acid (VPA), or 5 μM ATRA + 1 mM VPA for 6, 24, or 72 hours. Genome-wide expression profiling was performed using Affymetrix U133A microarrays. While cytotoxic chemotherapy remains the hallmark of cancer treatment, intensive regimens fall short in many malignancies, including high-risk neuroblastoma. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4685

35 Samples

Download data: CEL

(Submitter supplied) Chromatin immunoprecipitation sequencing of H3K4me2, H3K27ac as well as, ATACseq and RNA-seq reveals regulatory landscapes across different muscle groups, as well as in response to chronic exercise or muscle PGC1a overexpression. This work defines the unique enhancer repetoire of skeletal muscle in vivo and reveals that highly divergent exercise-induced or PGC1a-driven epigenomic programs direct partially convergent transcriptional networks.

Organism:

Mus musculus

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL19057

4 Samples

Download data: BEDGRAPH, TXT