Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE66087 | GEO | 2016/09/08

SECONDARY ACCESSION(S): PRJNA276177

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

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

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

2016-09-08 | GSE66244 | GEO

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

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

| PRJNA276180 | ENA

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-09-08 | GSE66245 | GEO

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

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

2016-09-08 | E-GEOD-66245 | biostudies-arrayexpress

Protein-protein interactions of BRG1 or BRG1-HSA in SW13 cells

Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.

2023-02-15 | PXD029647 | Pride

SUMO pulldown proteomics Namalwa 5-Aza-2' deoxycytidine treatment

Project description:Combination therapies targeting malignancies aim to increase treatment efficacy and reduce toxicity. Hypomethylating drug 5-Aza-2’-deoxycytidine (5-Aza-2’) enhances transcription of tumor suppressor genes and induces replication errors via entrapment of DNMT1. Post-translational modification by SUMO plays major roles in the DNA damage response and is required for degradation of entrapped DNMT1. Here, we combine SUMOylation inhibitor TAK981 and DNA-hypomethylating agent 5-Aza-2’ to improve treatment of MYC driven hematopoietic malignancies, since MYC overexpressing tumors are sensitive to SUMOylation inhibition. We studied the classical MYC driven malignancy Burkitt lymphoma, as well as diffuse large B-cell lymphoma (DLBCL) with and without MYC translocation. SUMO inhibition prolonged the entrapment of DNMT1 to DNA, resulting in DNA damage. An increase in DNA damage was observed in cells co-treated with TAK981 and 5-Aza-2’. Both drugs synergized to reduce cell proliferation in vitro in a B cell lymphoma cell panel, including Burkitt lymphoma and DLBCL. In vivo experiments combining TAK981 (25 mg/kg) and 5-Aza-2’ (2.5 mg/kg) showed a significant reduction in outgrowth of Burkitt lymphoma in an orthotopic xenograft model. In contrast, single dosing of TAK981 was ineffective and single dosing of 5-Aza-2’ only led to a modest outgrowth reduction. TAK981 and 5-Aza-2’ synergize to reduce B cell Lymphoma outgrowth in vitro and in vivo. SUMOylation is a key-player in the repair of DNA damage, hence upon TAK981 treatment the repair of DNA damage induced by 5-Aza-2’ treatment is impaired. Our results demonstrate the potential of tailored combination of drugs, based on insight in molecular mechanisms, to improve the efficacy of cancer therapies.

2023-03-17 | PXD038620 | Pride

Effects of SAHA on human gut microbiome

Project description:The human stool samples were collected and processed for in vitro culturing under anaerobic condition using rapidAIM assay with or without SAHA, an lysine deacetylase inhibitor, for evaluating the effects of SAHA on human gut microbiome. Metaproteomics were used to analyze the microbiome composition and functions.

2022-03-01 | PXD016388 | Pride

SAHA Rat Dental Pulp

Project description:Transcriptional response of rat dental pulp cells (DPCs) cultured with SAHA at early and late mineralisation time points Transcript profiling of DPC identified several novel genes expression induced and supressed by HDACi at 24 hrs and 14 days under mineralising conditions. SAHA induces several members of the MMP family of endopepsidases (TIMP-1, MMP-9, MMP-13) and other members of the endochondral ossification pathway at 24 h.

2015-06-16 | GSE67175 | GEO

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