Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

42 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Treatment with GC/RA and combination with AZA/SAHA in MYC amplified and BRG1 mutant lung cancer cell lines

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Manel Esteller

PROVIDER: E-GEOD-66245 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Patterns of changes in DNA global methylation following the treatment with GC/RA and with GC/RA plus AZA/SAHA in MYC amplified and BRG1 mutant lung cancer cell lines

Project description:Comprehensive characterization of the DNA methylome regulated by the treatment with glucocorticoids (GC) and retinoic acid (RA) alone and combined with AZA/SAHA and the relationship of these features with the status of BRG1 and MYC in lung cancer cell lines. MYC amplified cell lines and BRG1 mutant cell lines were treated with glucocorticoids (GC) and retinoic acid (RA) alone and combined with AZA/SAHA and their methylation was then measured

2016-09-08 | E-GEOD-66087 | biostudies-arrayexpress

Identification of expresion patterns after treatment with GC/RA and combination with AZA/SAHA in MYC amplified and BRG1 mutant lung cancer cell lines

Project description:To development our gene expression approach , we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the treatment with glucocorticoids (GC) and retinoic acid (RA) alone and combined with AZA/SAHA and the relationship of these features with the status of BRG1 and MYC in lung cancer cell lines. MYC amplified cell lines and BRG1 mutant cell lines were treated with glucocorticoids (GC) and retinoic acid (RA) alone and combined with AZA/SAHA and their expression was then measured

2016-09-08 | E-GEOD-66244 | biostudies-arrayexpress

AcceSssIble Assay to Study the Chomatin Accessibility and DNA Methylation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-03-08 | E-GEOD-38858 | biostudies-arrayexpress

AcceSssIble: an array-based assay for the study of chromatin accessibility and DNA methylation using the CpG methyltransferase SssI

Project description:Analysis of nucleosome positioning and chromatin state by using CpG methyltransferase M.SssI to methylate nuclei. Unmethylated regions that gain methylation (low to high beta value) are known to be accessible and nucleosome depleted. Intact nuclei are harvested from cells and treated with M.SssI. DNA is then extracted, bisulfite converted and run on an Infinium methylation array, along with a no-enzyme control. Background subtracted beta values (listed below) are used to determine regions that have gained methylation on enzyme treatment compared to the control - and these are used to infer chromatin state

2013-03-08 | E-GEOD-36580 | biostudies-arrayexpress

Functional DNA methylation is accompanied by chromatin accessibility [methylation]

Project description:Analysis of nucleosome positioning and chromatin state by using CpG methyltransferase M.SssI to methylate nuclei. Unmethylated regions that gain methylation (low to high beta value) are known to be accessible and nucleosome depleted. Method used to study changes after epigenetic drug treatments identified that majority of demethylation events are not accompanied by chromatin accessibility changes. Intact nuclei are harvested from cells and treated with M.SssI. DNA is then extracted, bisulfite converted and run on an Infinium methylation array, along with a no-enzyme control. Background subtracted beta values (listed below) are used to determine regions that have gained methylation on enzyme treatment compared to the control - and these are used to infer chromatin state

2013-03-08 | E-GEOD-43851 | biostudies-arrayexpress

Functional DNA methylation is accompanied by chromatin accessibility [gene expression]

2013-03-08 | E-GEOD-43852 | biostudies-arrayexpress

Transcription profiling of mouse C3H10T1/2 cells stimulated to differentiate using IDMB to investigate adipogenesis

Project description:Confluent C3H10T1/2 cells stimulated to differentiate using IDMB (1uM BRL49653, 1uM Dexamethasone, 0.5uM IBMX, 10ug/mL Insulin). Expression was examined 24 hours after IDMB treatment. Additionally, the effects of addition of TCDD 48 hours prior to IDMB treatment, and EGF addition concurrent with IDMB treatment were examined.

2007-12-14 | E-GEOD-1123 | biostudies-arrayexpress

Comparison of gene expression in Dnmt1+/+ MEFs treated with 5-aza-2'-deoxycytidine or vector control

Project description:DNA methylation and the Polycomb Repression System are epigenetic mechanisms that play important roles in maintaining transcriptional repression. Recent evidence suggests that DNA methylation can attenuate the binding of Polycomb protein components to chromatin and thus plays a role in determining their genomic targeting. However, whether this role of DNA methylation is important in the context of transcriptional regulation is unclear. By genome-wide mapping of the Polycomb Repressive Complex 2 (PRC2)-signature histone mark, H3K27me3, in severely DNA hypomethylated mouse somatic cells, we show that hypomethylation leads to widespread H3K27me3 redistribution, in a manner that reflects the local DNA methylation status in wild-type cells. Unexpectedly, we observe striking loss of H3K27me3 and PRC2 from Polycomb-target gene promoters in DNA hypomethylated cells, including Hox gene clusters. Importantly, we show that many of these genes become ectopically expressed in DNA hypomethylated cells, consistent with loss of Polycomb-mediated repression. An intact DNA methylome is required for appropriate Polycomb-mediated gene repression by constraining PRC2 targeting. These observations identify a previously unappreciated role for DNA methylation in gene regulation and therefore influence our understanding of how this epigenetic mechanism contributes to normal development and disease. Two biological replicates are compared, each consisting of two technical replicates

2013-02-12 | E-GEOD-44276 | biostudies-arrayexpress

Transcription profiling of human MCF-7 cells treated with proteasome inhibitor MG132 and either dexamethasone or 17b-estradiol

Project description:The objective of the study was to investigate the effect of proteasome inhibition on glucocorticoid and estrogen receptor regulated gene expression. Experiment Overall Design: MCF-7 cells were treated with proteasome inhibitor (MG132), dexamethasone, 17b-estradiol or MG132 plus dexamethasone or MG132 plus 7b-estardiol. Control cells were not treated. RNA was collected from 2 biological experiments.

2008-06-20 | E-GEOD-8383 | biostudies-arrayexpress

Distinct Patterns of DNA Methylation and Transcript Isoform Regulation in Prostate Cancer

Project description:Methylation profiling of human prostate cancer tissues and cell lines. We mapped the global DNA methylation patterns in prostate tissues (n=17) and cells (n=2) from fifty nanograms of genomic DNA using Methylplex-Next Generation Sequencing (M-NGS). In addition, genes methylated in LNCaP and significantly overexpressed after 5’Azacytidine treatment of LNCaP cells are assessed by Agilent gene expression microarray. The comprehensive methylome map presented here will further our understanding of epigenetic regulation of the prostate cancer genome. [Gene expression] Two-condition experiment, control DMSO-treated vs. 5'aza-treated LNCaP at two time points (@24 and 48 hours) in replicates.

2010-11-15 | E-GEOD-25346 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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