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RNA-seq of SUPT1, LOUCY, JURKAT and DND41 after treatment with 5-azacytidine and Vitamin C

ABSTRACT: RNA-seq of SUPT1, LOUCY, JURKAT and DND41 after treatment with 5-azacytidine and Vitamin C

PROVIDER: PRJEB45270 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5968760_1.fastq.gz	Fastqsanger.gz
	ERR5968760_2.fastq.gz	Fastqsanger.gz
	ERR5968770_1.fastq.gz	Fastqsanger.gz
	ERR5968770_2.fastq.gz	Fastqsanger.gz
	ERR5968780_1.fastq.gz	Fastqsanger.gz

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RNA-seq of SUPT1, LOUCY, JURKAT and DND41 after treatment with 5-azacytidine and Vitamin C

Project description:TET2 is a know tumorsuppressor gene involved in the demethylation of DNA. TET2 catalyses the conversion of 5-methyl cytosine (5-mC) to 5-hydroximethyl cytosine (5-hmC), an important step in the removal of methylation from the DNA. In T-All mutations in TET2 are rare, however we have found that it is often silenced by DNA Methylation. 5-Azacytidine (5-AZA) is a an effective demethylating agent used as a cancer treatment and has been showed to be able to reactivate methylated genes. Similarly, Vitamin C is an important co-factor for TET2 and has been shown to have synergistic effects with 5-Azacytidine. By treating the TET2 methylated T-ALL cell lines Loucy and DND41 and comparing to TET2 expressing T-ALL cells lines such as SUP-T1 and Jurkat we aimed to explore if 5-AZA could reactivate TET2 in T-ALL, what effects this would have on tumorgenicity and whether Vitamin C had any synergy with these effects in T-ALL. As part of this effort we treated the cell lines SUP-T1, Jurkat, Loucy and DND41 with 5-AZA and Vitamin C and performed Total RNA-seq to explore the effects of 5-AZA and Vitamin C on the expression of genes and non-coding elements such as retrotransponsons.

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Project description:Here we performed low coverage whole genome enzymatic-mehtyl-conversion sequencing (EM-seq) of 11 commercially available T-ALL cell lines to evaluate their global DNA methylation profile. We then proceeded to treat ALL-SIL, SUP-T1, LOUCY and JURKAT with varying concentrations (0-3000 nM) of three different hypomethylating agents, 5-azacytidine (AZA), 5-aza-2′-deoxycytidine (DEC) and GSK3685032 (GSK5032), for 3 and 7 days to evaluate their DNA demethylating ability.

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Project description: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

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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.

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