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Gene regulation in Erbb2 transfected NIH3T3 cells after Azacytidine treatment

ABSTRACT: 5-Azacytidine or 5-aza-2’-deoxycytidine is a chemical analogue of the cytosine nucleoside used in DNA and RNA. Cells in the presence of 5-azacytidine incorporate it into DNA during replication and RNA during transcription. The incorporation of 5-azacytidine into DNA or RNA inhibits methyltransferase thereby causing demethylation in that sequence, affecting the way that cell regulation proteins are able to bind to the DNA/RNA substrate. Inhibition of DNA occurs through the formation of stable complexes between the molecule and with DNA methyltransferases, thereby saturating the cells methylation machinery. 5-azacytidine is mainly used in the treatment of myelodysplastic syndrome. Changes in gene expression levels in Erbb2 transfected murine fibroblast cell line after treatment with Azacytidine in two different concentrations were analysed. Keywords: cDNA microarray, murine fibroblast, azacytidine treatment, carcinogenesis

ORGANISM(S): Mus musculus

PROVIDER: GSE8374 | GEO | 2009/10/01

SECONDARY ACCESSION(S): PRJNA101407

REPOSITORIES: GEO

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Gene regulation in Erbb2 transfected NIH3T3 cells after Azacytidine treatment

Project description:5-Azacytidine or 5-aza-2â??-deoxycytidine is a chemical analogue of the cytosine nucleoside used in DNA and RNA. Cells in the presence of 5-azacytidine incorporate it into DNA during replication and RNA during transcription. The incorporation of 5-azacytidine into DNA or RNA inhibits methyltransferase thereby causing demethylation in that sequence, affecting the way that cell regulation proteins are able to bind to the DNA/RNA substrate. Inhibition of DNA occurs through the formation of stable complexes between the molecule and with DNA methyltransferases, thereby saturating the cells methylation machinery. 5-azacytidine is mainly used in the treatment of myelodysplastic syndrome. Changes in gene expression levels in Erbb2 transfected murine fibroblast cell line after treatment with Azacytidine in two different concentrations were analysed. Keywords: cDNA microarray, murine fibroblast, azacytidine treatment, carcinogenesis Gene expression levels of Erbb2 transfected NIH3T3 cell lines treated with 5ÂµM and 10ÂµM Azacytidine were compared to Erbb2 transfected but non-treated NIH3T3 cell line. For each Azacytidine concentration 4-8 experiments were performed including 50% dye swaps. As a controll experiments gene expression levels of NIH3T3 cells with and without Azacytidine treatment were analysed

2009-10-01 | E-GEOD-8374 | biostudies-arrayexpress

5-azacytidine treatment reorganizes genomic histone modification patterns

Project description:Methylation of DNA in combination with histone modifications establishes an epigenetic code that ensures the proper control of gene expression. Although DNA methyltransferases have been shown to interact with histone methyltransferases such as EZH2 (which methylates histone H3 on lysine 27) and G9a (which methylates histone H3 on lysine 9), the relationship between DNA methylation and repressive histone marks has not been fully studied. In cancer cells, promoters of genes are often aberrantly methylated. Accordingly, 5-azacytidine (a DNA demethylating drug) is used for treating patients with myelodysplastic syndrome. However, no genome-scale studies of the effects of this drug have been reported. In this work, we report the effects of 5-azacytidine on global gene expression and analyze ~24,000 human promoters using ChIP-chip to determine how 5-azacytidine treatment effects H3K27me3 and H3K9me3 levels. We found that (1) 5-azacytidine treatment results in large changes in gene regulation with distinct functional categories of genes showing increased (e.g. C2H2 zinc finger transcription factors) and decreased (e.g. genes involved in regulation of mitochondria and oxidoreductase activity) levels; (2) most genes that show altered expression are not regulated by promoters that display DNA methylation prior to the treatment; (3) certain gene classes switch their repression mark upon treatment with 5-azacytidine (from H3K27me3 to H3K9me3 and vice versa); and (4) most changes in gene expression are not due to relief of repression mediated by DNA or histone methylation.

2010-04-09 | GSE20598 | GEO

5-azacytidine treatment reorganizes genomic histone modification patterns

2010-04-09 | E-GEOD-20598 | biostudies-arrayexpress

Escherichia coli: untreated versus 5-azacytidine-treated expression profiles

Project description:DNA microarray experiments were used to compare gene expression profiles of untreated and 5-azacytidine treated Escherichia coli at both logarithmic phase and early stationary phase The goal was to determine the effect of cytosine DNA methylation loss on gene expression (5-azacytidine is a methylation inhibitor)

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Epigenome analysis of U937, U937 treated with 5mM azacytidine for 24 and 72 hours and its azacytidine-resistant derivative

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RNAseq to investigate transcriptional changes in human MM cell lines due to panobinostat, 5-Azacytidine, panobinostat+5-Azacytidine or n-methyl-2-pyrroldine (NMP) treatments.

Project description:Purpose: We applied RNA sequencing technology for high-throughput analysis of transcriptional changes within human MM cell lines JJN3 and U266 due to individual and combination drug treatment. Methods: JJN3 and U266 cells were treated with pan-HDACi panbobinostat, DNMTi 5-Azacytidine, panobinostat+5-Azacytidine or NMP for 4h or 24h in triplicate and transcriptional changes assessed by RNAseq using Illumina HiSeq platform. Specifically, JJN3 cells were treated with 10nM panobinostat, 2.5µM 5-Azacytidine, panobinostat+5-Azacytidine (at given doses), or 10mM NMP. U266 cells were treated with 10nM panobinostat, 10µM 5-Azacytidine, panobinostat+5-Azacytidine (at given doses), or 10mM NMP. Results: We report unique and overlapping transcriptional signatures that lead to the induction of apoptosis in human MM cell lines in a cell-specific manner due to individual or combination treatments. Conclusions: A detailed analysis of differential transcriptional events in human MM cell lines due to HDACi, DNMTi, HDACi+DNMTi and NMP appear to define the molecular events leading to apoptosis and drug mechanism of action.

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miRNA expression profiling of Human Myeloma Cell Lines Pre- and Post- 5'azacytidine Treatment

Project description:We performed genome-wide miRNA expression profiling (MEP) of a panel of four human Myeloma cell lines treated with 5'azacytidine compared to control (DMSO treatment), with the objective of unmasking miRNAs silenced by DNA hypermethylation.

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Bisulfite (methylome) sequencing of msh1 memory line treated with 5-azacytidine in Arabidopsis

Project description:Germination of the memory line and isogenic Col-0 wild type on media containing 100 uM 5-azacytidine alleviated the phenotype differences between the two lines, resulting in similar growth rates. Here we generate methylome profile for wild type and msh1 memory line under 100 uM 5-azacytidine treatment to investigate the effect of 5-azacytidine on msh1 memory line methylation profile.

2019-05-18 | GSE114665 | GEO

Effect of 5-azacytidine on gene expression in C2C12 myoblasts

Project description:Mesenchymal progenitor cells can be differentiated in vitro into myotubes that exhibit many characteristic features of primary mammalian skeletal muscle fibers. However, in general, they do not show the functional excitation-contraction coupling or the striated sarcomere arrangement typical of mature myofibers. Epigenetic modifications have been shown to play a key role in regulating the progressional changes in transcription necessary for muscle differentiation. In this study, we demonstrate that treatment of murine C2C12 mesenchymal progenitor cells with 10 µM of the DNA methylation inhibitor 5-azacytidine (5AC) promotes myogenesis, resulting in myotubes with enhanced maturity as compared to untreated myotubes. Specifically, 5AC treatment resulted in the upregulation of muscle genes at the myoblast stage while at later stages nearly 50 % of the 5AC-treated myotubes displayed a mature, well-defined sarcomere organization as well as spontaneous contractions that coincided with action potentials and intracellular calcium transients. Both the percentage of striated myotubes and their contractile activity could be inhibited by 20 nM TTX, 10 µM ryanodine and 100 µM nifedipine, suggesting that action potential-induced calcium transients are responsible for these characteristics. Our data suggest that genomic demethylation induced by 5AC overcomes an epigenetic barrier that prevents untreated C2C12 myotubes from reaching full maturity. C2C12 cells were plated at 1500 cells/cm2 (day -1), cultured for 1 day in DMEM 10%NCS, then treated (d0) with or without 10uM 5-azacytidine (5AC) for an additional 3 days. RNA was extracted on day 3 and hybridized to GeneChip Mouse Genome 430 2.0 array (Affymetrix).

2012-01-01 | E-GEOD-30192 | biostudies-arrayexpress

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