Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of butyrate and DZNep on hESC HSF-6

ABSTRACT: In order to recover nuclei with two active X chromosomes (class I), we developed a reprogramming strategy by supplementing hESC media with the small molecules sodium butyrate, and 3-deazaneplanocin A (DZNep). In order to determine how B+D affects global gene expression, we performed microarray analysis in triplicate in the HSF-6 (8) C and HSF-6 (8) B+D treated cultures. We also evaluated HSF-6 (S9) B+D in triplicate and identified no statistically significant changes in gene expression in HSF-6 (S9) B+D compared to HSF-6 (8) B+D treated cultures. This suggests that global transcriptional differences are more strongly modulated by presence or absence of B+D and not the percentage of class I, II or III nuclei.

ORGANISM(S): Homo sapiens

PROVIDER: GSE33864 | GEO | 2011/11/22

SECONDARY ACCESSION(S): PRJNA148153

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Effect of butyrate and DZNep on hESC HSF-6

Project description:In order to recover nuclei with two active X chromosomes (class I), we developed a reprogramming strategy by supplementing hESC media with the small molecules sodium butyrate, and 3-deazaneplanocin A (DZNep). In order to determine how B+D affects global gene expression, we performed microarray analysis in triplicate in the HSF-6 (8) C and HSF-6 (8) B+D treated cultures. We also evaluated HSF-6 (S9) B+D in triplicate and identified no statistically significant changes in gene expression in HSF-6 (S9) B+D compared to HSF-6 (8) B+D treated cultures. This suggests that global transcriptional differences are more strongly modulated by presence or absence of B+D and not the percentage of class I, II or III nuclei. We performed gene expression profiling on hESC HSF-6 (8, S9) in absent (control) and presence of butyrate and DZNep. All cell were collected after 11 passages in absent and presence of butyrate and DZNep.

2011-11-22 | E-GEOD-33864 | biostudies-arrayexpress

DMSO control and DZNep treated MOLM-14 cells

Project description:We demonstrated that 3-Deazaneplanocin A (DZNep), a histone methyltransferase inhibitor, induce robust apoptosis in AML cells through increased ROS production and ER stress. We identified a core gene signature including TXNIP, a major redox control molecule which is crucial in DZNep-induced apoptosis.

2011-07-01 | GSE30315 | GEO

DMSO control and DZNep treated MOLM-14 cells

2011-07-01 | E-GEOD-30315 | biostudies-arrayexpress

Vitamin C promotes anti-leukemia of DZNep in Acute Myeloid Leukemia

Project description:The epigenetic treatment by 3-Deazaneplanocin A (DZNep), a histone methyltransferase inhibitor, shows great potential against acute myeloid leukemia (AML). However, the variant sensitivity and incomplete response to DZNep are commonly observed. We reveal that vitamin C (Vc) dramatically promotes DZNep response against leukemic cells in different cell lines and primary AML samples. To examine the molecular determinants underlying Vc enhanced anti-leukemia effect of DZNep, we conducted a genome-wide RNA sequencing and a gene ontology (GO) enrichment analysis of differentially expressed mRNAs in each group was performed.

2022-09-30 | GSE192629 | GEO

Real-time quantitative PCR analysis of DZNep treated B cell Lymphoma cell line Jeko-1

Project description:Jeko-1 cells were culture with or without PRC2 inhibitor 3-deazaneplanocin A (DZNep)(1uM) for 72hrs. We used TaqMan® Human MicroRNA Array to quantitate miRNA expression profile regulated by PRC2.

2012-08-11 | GSE40019 | GEO

Effects of DZNep and 5-Aza-CdR on gene expression in MCF7 cells

Project description:DNA methylation, histone modifications, and nucleosomal occupancy collaborate to cause silencing of tumor related genes in cancer. The development of drugs that target these processes is therefore important for cancer therapy. Inhibitors of DNA methylation and histone deacetylation have already been approved by the FDA for the treatment of hematologic malignancies. However, drugs that target the other mechanisms still need to be developed. Recently, 3-deazaneplanocin A (DZNep) was reported to selectively inhibit the trimethylation of lysine 27 on histone H3 (H3K27me3) and lysine 20 on histone H4 (H4K20me3) as well as re-activate silenced genes in cancer cells. This finding opens the door to pharmacological inhibition of histone methylation and we therefore wanted to further study the mechanism of action of 3-deazaneplanocin A in cancer cells. Western blot analysis showed that two other drugs, sinefungin and adenosine-dialdehyde (Adox), have similar effects on the trimethylation H3K27 as 3-deazaneplanocin A and that DZNep is not selective, but globally inhibits histone methylation. Intriguingly, chromatin immunoprecipitation of various histone modifications and microarray analysis show DZNep acts via a different pathway to 5-aza-2´-deoxycytidine (5-azaCdR), a DNA methyltransferase inhibitor and gives us an interesting insight into how chromatin structure effects gene expression. We also determine the kinetics of gene activation in order to understand if the induced changes were somatically heritable. We have found that upon removal of DZNep, gene expression is reduced to its original state suggesting that there is a homeostatic mechanism which returns the histone modifications to their “ground state” after DZNep treatment. Not only do these studies show the strong need for further development of histone methylation inhibitors but also allow us to better understand how chromatin structure affects gene expression.

2009-03-01 | GSE13733 | GEO

Real-time quantitative PCR analysis of DZNep treated B cell Lymphoma cell line Jeko-1

Project description:Jeko-1 cells were culture with or without PRC2 inhibitor 3-deazaneplanocin A (DZNep)(1uM) for 72hrs. We used TaqManM-BM-. Human MicroRNA Array to quantitate miRNA expression profile regulated by PRC2. qPCR miRNA expression profiling.

2012-08-11 | E-GEOD-40019 | biostudies-arrayexpress

The S-adenosyl-homosteine hydrolase inhibitor DZNeP unspecifically affects histone methylation patterns in embryos and results in developmental aberrations

Project description:3-deazaneplanocin A (DZNeP) is a promising cancer drug affecting the methylation status of histone lysine residues. To investigate the specificity and mode of action of DZNeP, zebrafish embryos displaying high histone methyltransferase activity were cultured with DZNeP and histone methylation (H3K4me3, H3K9me3, H3K27me3) was mapped by ChIP-chip genome-wide promoter at post-MBT stage (5.3 hpf) . We used a custom 2.1M probe HD promoter array (Nimblegen) for ChIP and input DNA hybridization. Peak detection was done using MA2C with P=10e-4 as cutoff.

2014-11-21 | GSE53209 | GEO

Effects of DZNep and 5-Aza-CdR on gene expression in MCF7 cells after 72 h treatment

2009-03-24 | GSE15200 | GEO

shRNA profiling of human DZNep-treated glioblastoma multiforme cancer stem cells

Project description:Overexpression of the Polycomb group protein Enhancer of Zeste Homolog 2 (EZH2) occurs in diverse malignancies, including prostate cancer, breast cancer, and glioblastoma multiforme (GBM) (1). Based on its ability to modulate transcription of key genes implicated in cell cycle control, DNA repair and cell differentiation, EZH2 is believed to play a crucial role in tissue-specific stem cell maintenance and tumor development. Here we show that targeted pharmacologic disruption of EZH2 by the S-adenosylhomocysteine hydrolase inhibitor 3-Deazaneplanocin A (DZNep), or its specific down-regulation by shRNA, strongly impairs GBM cancer stem cell self-renewal in vitro and tumor-initiating capacity in vivo. Using genome-wide expression analysis of DZNep-treated GBM cancer stem cells, we found the expression of c-myc, recently reported to be essential for GBM cancer stem cells, to be strongly repressed upon EZH2 depletion. Specific shRNA-mediated down-regulation of EZH2 in combination with chromatin immunoprecipitation (ChIP) experiments revealed that c-myc is a direct target of EZH2 in GBM cancer stem cells. Taken together, our observations provide evidence that direct transcriptional regulation of c-myc by EZH2 may constitute a novel mechanism underlying GBM cancer stem cell maintenance and suggest that EZH2 may be a valuable new therapeutic target for GBM management. Experiment Overall Design: Three samples of cancer stem-cell enriched gliospheres from primary glioblastoma multiforme cell cultures were treated with DZNep. Untreated gliospheres from the same cultures were used as controls.

2009-12-14 | E-GEOD-18150 | 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