Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MiR expression microarray analysis on M2 macrophages treated with epigenetic modifiers

ABSTRACT: Epigenetic regulation of gene expression involves DNA methylation, histone methylation or acetylation, and microRNA (miRNA)-mediated mRNA degradation. We studied, if epigenetic modifiers namely 5-aza-2'-deoxycytidine and trichostatin A could remodulate the miR expression in M2 macrophage and enable M2-M1 reprogramming.

ORGANISM(S): Mus musculus synthetic construct

PROVIDER: GSE218160 | GEO | 2022/11/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Role of epigenetic modifiers on the bovine fibroblast innate immune response

Project description:The innate immune signaling pathway plays a crucial role in the recognition and early response to pathogens associated with disease. Genetic analysis has been unable to completely account for individual variability in the strength of the innate immune response. The aim of this study was to determine the role of the epigenetic markers (DNA methylation or histone acetylation) in controlling bovine gene expression in relation to the response to lipopolysaccharide (LPS). To determine the impact epigenetics may have in controlling innate immunity, dermal fibroblasts from fifteen dairy heifers having previously displayed a differential response to LPS were exposed to 5-aza-2M-bM-^@M-^Y-deoxyctidine (AZA) and trichostatin A (TSA); de-methylating and hyper-acetylating agents, respectively. The AZA-TSA Fibroblast cultures (n=3) were examined under either control conditions or for gene expression following epigenetic modification with the de-methylating agent 5-aza-2'-deoxycytidine and hyper-acetylation agent trichostatin-A. Finally, expression was investigated for responsiveness to lipopolysaccharide (LPS)

2014-01-01 | E-GEOD-50405 | biostudies-arrayexpress

RNA-seq of head and neck cancer cell lines

Project description:Transcriptome analysis in head and neck cancer cell lines, FaDu and UMSCC47 with and without 5-aza'2-deoxycytidine(Aza)/trichostatin A(TSA) treatment.

2018-05-10 | GSE98805 | GEO

DNA methylation analysis in head and neck cancer cells

Project description:DNA methylation analysis in oropharyngeal squamous carcinoma(OPSCC) samples, oropharyngeal non-cancerous mucosa samples and head and neck cancer cell lines, FaDu and UMSCC47 before and after 5-aza'2-deoxycytidine(Aza)/trichostatin A(TSA) treatment. Infinium HumanMethylation450 BeadChip was used to obtain DNA methylation profiles across 485,577 CpG sites. Samples included 13 OPSCC samples, 4 non-cancerous mucosa samples and 2 FaDu with and without Aza/TSA treatment and 2 UMSCC47 with and without Aza/TSA treatment.

2018-05-10 | GSE98807 | GEO

Transcription profiling of three human multiple myeloma cell lines treated with 5-aza-2-deoxycytidine and/or trichostatin A

Project description:To identify epigenetically silenced genes in multiple myeloma (MM) cell lines and to determine the effects of 5-aza-2-deoxycytidine and trichostatin A on gene expression. We treated 3 multiple myeloma cell lines (MM1, NCI-H929, U266) with 5-aza-2-deoxycytidine and/or trichostatin A.

2008-02-01 | E-MEXP-1269 | biostudies-arrayexpress

Role of epigenetic modifiers on the bovine fibroblast innate immune response

Project description:The innate immune signaling pathway plays a crucial role in the recognition and early response to pathogens associated with disease. Genetic analysis has been unable to completely account for individual variability in the strength of the innate immune response. The aim of this study was to determine the role of the epigenetic markers (DNA methylation or histone acetylation) in controlling bovine gene expression in relation to the response to lipopolysaccharide (LPS). To determine the impact epigenetics may have in controlling innate immunity, dermal fibroblasts from fifteen dairy heifers having previously displayed a differential response to LPS were exposed to 5-aza-2’-deoxyctidine (AZA) and trichostatin A (TSA); de-methylating and hyper-acetylating agents, respectively. The AZA-TSA

2014-01-01 | GSE50405 | GEO

miR expression microarray analysis on M2 macrophages treated with epigenetic modifiers

Project description:miR expression microarray analysis on M2 macrophages treated with epigenetic modifiers

| PRJNA902567 | ENA

IFN-γ and IL-4 regulate epigenetic modifiers in macrophages

Project description:Interferon-γ (IFN-γ) or interleukin-4 (IL-4) prime macrophages towards classical (M1) or alternative (M2) activation, respectively. How IFN-γ and IL-4 prime epigenetic responses by altering expression of histone modifying enzymes and how this affects M1/M2 polarization is incompletely understood.

2017-01-15 | GSE83957 | GEO

5Aza and TSA treatment of MCF7 cells (BS-seq)

Project description:The goal of this study is to identify the DNA methylation changes caused by exposure of to the DNMT inhibitor 5-aza-2â-deoxycytidine (5Aza) and HDAC inhibitor Trichostatin A (TSA). We performed whole-genome bisulfite sequencing of the drug-treated MCF7 breast cancer cell lines and compare their DNA methylation profile with the untreated MCF7 (see E-MTAB-2014). While MCF7 treated with both drugs experienced global loss of DNA methylation, the 5Aza induced stronger demethylation than TSA.

2016-06-30 | E-MTAB-3785 | biostudies-arrayexpress

Identification of epigenetically silenced genes in tumor endothelial cells

Project description:Tumor angiogenesis requires intricate regulation of gene expression in endothelial cells (EC). We recently showed that DNA methyltransferase (DNMT)- and histone deacetylase (HDAC) inhibitors directly repress EC growth and tumor angiogenesis, suggesting that epigenetic modifications mediated by DNMTs and HDACs are involved in regulation of EC gene expression during tumor angiogenesis. To understand the mechanisms behind the epigenetic regulation of tumor angiogenesis, we used microarray analysis to perform a comprehensive screen to identify genes downregulated in tumor-conditioned versus quiescent EC, and re-expressed by 5-aza-2’-deoxycytidine and trichostatin A. Among the 81 genes identified, 77% harboured a promoter CpG island. Validation of mRNA levels of a subset of genes confirmed significant downregulation in tumor-conditioned EC and reactivation by treatment with a combination of 5-aza-2’-deoxycytidine and trichostatin A, as well as by both compounds separately. Silencing of these genes in tumor-conditioned EC correlated with promoter histone H3 deacetylation and loss of H3 lysine 4 methylation, however did not involve DNA methylation of promoter CpG islands. For six genes, downregulation in microdissected human tumor endothelium was confirmed. Functional validation by RNA interference revealed that clusterin, fibrillin 1 and quiescin Q6 are negative regulators of EC growth and angiogenesis. In summary, our data identify novel angiogenesis suppressing genes which become silenced in tumor-conditioned EC in association with promoter histone modifications and reactivated by DNMT- and HDAC inhibitors through reversal of these epigenetic modifications, providing a mechanism for epigenetic regulation of tumor angiogenesis. Keywords: treated versus untreated

2007-02-28 | GSE7132 | GEO

Genome-wide microRNA expression profiling identifies miR-9-3 and miR-193a as targets for DNA methylation in non-small cell lung cancers

Project description:Purpose: The major aim of this study was to investigate the role of DNA methylation (referred to as methylation) on microRNA (miRNA) silencing in non-small cell lung cancers (NSCLC). Experimental Design: We performed microarray expression analyses of 856 miRNAs in NSCLC A549 cells before and after treatment with the DNA methyltransferase inhibitor 5-aza-2Â´-deoxycytidine (Aza-dC) and with a combination of Aza-dC and the histone deacetylase inhibitor trichostatin A. MiRNA methylation was determined in 11 NSCLC cell lines and in primary tumors and corresponding non-malignant lung tissue samples of 101 stage I-III NSCLC patients. Results: By comparing microarray data of untreated and drug treated A549 cells, we identified 33 miRNAs whose expression was upregulated after drug treatment and which are associated with a CpG island. Thirty (91%) of these miRNAs were found to be methylated in at least 1 of 11 NSCLC cell lines analysed. Moreover, miR-9-3 and miR-193a were found to be tumor-specifically methylated in NSCLC patients. We observed a shorter disease-free survival of miR-9-3 methylated lung squamous cell carcinoma (LSCC) patients compared to miR-9-3 unmethylated LSCC patients by multivariate analysis (HR = 3.8, 95% CI = 1.3 to 11.2, p = 0.017) and a shorter overall survival of miR-9-3 methylated LSCC patients compared to miR-9-3 unmethylated LSCC patients by univariate analysis (p = 0.013). Conclusions: Overall, our results suggest that methylation is an important mechanism for inactivation of certain miRNAs in NSCLCs and that miR-9-3 methylation may serve as a prognostic parameter in LSCC patients. MiRNA expression (LC Sciences, mirBASE12) was analyzed before and after treatment of A549 cells with 5-aza-2Â´-deoxycytidine (Aza-dC) and a combination of Aza-dC and trichostatin A (TSA). Experiments were performed in duplicates.

2012-03-13 | E-GEOD-31579 | 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