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Metabolic regulation by p53 prevents R-loop-associated genomic instability [ATAC-Seq]

ABSTRACT: To investigate the role of p53 in maintaining genome integrity we deleted p53 via doxycycline-inducible short hairpin (sh)RNA targeting p53 (KPshp53 cells), and we treat the cells with the DNA demethylating molecule 5-Aza-2′-deoxycytidine (AZA or dC)

ORGANISM(S): Mus musculus

PROVIDER: GSE207878 | GEO | 2022/08/24

REPOSITORIES: GEO

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Metabolic regulation by p53 prevents R-loop-associated genomic instability [RNA-Seq]

Project description:To investigate the role of p53 in maintaining genome integrity we deleted p53 via doxycycline-inducible short hairpin (sh)RNA targeting p53 (KPshp53 cells), and we treat the cells with the DNA demethylating molecule 5-Aza-2′-deoxycytidine (AZA or dC)

2022-08-24 | GSE207879 | GEO

Genome-wide DNA demethylation of TGW (neuroblastoma cell line) after treatment of mock and 5-aza-2'-deoxycytidine (5-aza-dC)

Project description:A neuroblasoma cell line, TGW, was treated with a DNA demethylating agents (5-aza-2'-deoxycytidine: 5-aza-dC). Genome-wide DNA methylation was analyzed using the Infinium Human MethylationEPIC BeadChip.

2021-07-23 | GSE180660 | GEO

Genome-wide DNA demethylation of NB-1 (neuroblastoma cell line) after treatment of mock and 5-aza-2'-deoxycytidine (5-aza-dC)

Project description:A neuroblasoma cell line, NB-1, was treated with a DNA demethylating agents (5-aza-2'-deoxycytidine: 5-aza-dC). Genome-wide DNA methylation was analyzed using the Infinium HumanMethylation450 BeadChip.

2021-07-29 | GSE180929 | GEO

Acute hypersensitivity of pluripotent testicular cancer-derived embryonal carcinoma to low-dose 5-aza deoxycytidine (part 1)

Project description:Human embryonal carcinoma (EC) cells are the stem cells of nonseminoma testicular germ cells tumors (TGCTs) and share remarkable similarities to human embryonic stem (ES) cells. In prior work we found that EC cells are hypersensitive to low nanomolar doses of 5-aza deoxycytidine (5-aza) and that this hypersensitivity partially depended on unusually high levels of the DNA methyltransferase, DNMT3B. We show here that low-dose 5-aza treatment results in DNA damage and induction of p53 in NT2/D1 cells. In addition, low-dose 5-aza results in global and gene specific promoter DNA hypomethylation. Low-dose 5-aza induces a p53 transcriptional signature distinct from that induced with cisplatin in NT2/D1 cells and also uniquely downregulates genes associated with pluripotency including NANOG, SOX2, GDF3 and Myc target genes. Changes in the p53 and pluripotency signatures with 5-aza were to a large extent dependent on high levels of DNMT3B. In contrast to the majority of p53 target genes upregulated by 5-aza that did not show DNA hypomethylation, several other genes induced with 5-aza had corresponding decreases in promoter methylation. These genes include RIN1, SOX15, GPER, and TLR4 and are novel candidate tumors suppressors in TGCTs. Our studies suggest that the hypersensitivity of NT2/D1 cells to low-dose 5-aza is multifactorial and involves the combined activation of p53 targets, repression of pluripotency genes, and activation of genes repressed by DNA methylation. Low-dose 5-aza therapy may be a general strategy to treat those tumors that are sustained by cells with embryonic stem-like properties. Total RNA obtained from NT2/D1-R1 sh control or NT2/D1-R1 sh DNMT3B knockdown cells treated with vehicle or 10 nM 5-aza deoxycytidine for 3 days. Four groups in biological triplicate for total of 12 hybridizations on Illumina HT-12v3 beadarray.

2012-12-01 | E-GEOD-42644 | biostudies-arrayexpress

Acute hypersensitivity of pluripotent testicular cancer-derived embryonal carcinoma to low-dose 5-aza deoxycytidine (part 3)

Project description:Human embryonal carcinoma (EC) cells are the stem cells of nonseminoma testicular germ cells tumors (TGCTs) and share remarkable similarities to human embryonic stem (ES) cells. In prior work we found that EC cells are hypersensitive to low nanomolar doses of 5-aza deoxycytidine (5-aza) and that this hypersensitivity partially depended on unusually high levels of the DNA methyltransferase, DNMT3B. We show here that low-dose 5-aza treatment results in DNA damage and induction of p53 in NT2/D1 cells. In addition, low-dose 5-aza results in global and gene specific promoter DNA hypomethylation. Low-dose 5-aza induces a p53 transcriptional signature distinct from that induced with cisplatin in NT2/D1 cells and also uniquely downregulates genes associated with pluripotency including NANOG, SOX2, GDF3 and Myc target genes. Changes in the p53 and pluripotency signatures with 5-aza were to a large extent dependent on high levels of DNMT3B. In contrast to the majority of p53 target genes upregulated by 5-aza that did not show DNA hypomethylation, several other genes induced with 5-aza had corresponding decreases in promoter methylation. These genes include RIN1, SOX15, GPER, and TLR4 and are novel candidate tumors suppressors in TGCTs. Our studies suggest that the hypersensitivity of NT2/D1 cells to low-dose 5-aza is multifactorial and involves the combined activation of p53 targets, repression of pluripotency genes, and activation of genes repressed by DNA methylation. Low-dose 5-aza therapy may be a general strategy to treat those tumors that are sustained by cells with embryonic stem-like properties. Genomic DNA obtained from NT2/D1-R1 sh control or NT2/D1-R1 sh DNMT3B knockdown cells treated with vehicle or 10 nM 5-aza deoxycytidine for 3 days. Four groups in biological triplicate for total of 12 hybridizations on Illumina HumanMethylation27 BeadChip.

2012-12-01 | E-GEOD-42646 | biostudies-arrayexpress

Genome-wide gene expression of NB-1 after treatment of 5-aza-dC, TBT, and combination

Project description:A neuroblastoma cell line, NB-1, was treated with mock, a DNA demethylating agent (5-aza-2'-deoxycytidine: 5-aza-dC), a synthetic retinoic acid (tamibarotene: TBT), and the combination of 5-aza-dC and TBT. A genome-wide gene expression analysis was performed using SurePrint G3 Human Gene Expression 8 x 60K v2 Microarray.

2021-07-23 | GSE180645 | GEO

Finding genetic loci that are sensitive to demethylation to assist in the development of DNA methylation-based in vitro assay for the identification of carcinogens

Project description:Purpose: To use reduced representation bisulfite sequencing and RNA-seq to identify demethylated promoters of genes that were derepressed following treatment with demethylating agent, 5-Aza-2'-deoxycytidine (5aCdR, CAS# 2353-33-5).

2023-02-10 | GSE218911 | GEO

mRNA profile of 5-aza-CR and 5-aza-CdR treated celllines

Project description:5-azacytidine and 5-aza-2'-deoxycytidine are both demethylating agents but they have shown different clinical efficiency. Since 5-azacytidine is incorporated into RNA it might have a different impact on the expression profile than 5-aza-2'-deoxycytidine. This study is designed to investigate the immediate action of the DNMTi on day 2 and the late heritable effects on day 8 after start of treatment.

2014-06-13 | E-MTAB-280 | biostudies-arrayexpress

Improved DNA methylation analysis via enrichment of demethylated cells expressing an X-inactivated GFP transgene

Project description:The demethylating drug 5-aza-2’-deoxycytidine (5-aza-2dC) is frequently used to investigate the effect of global DNA demethylation on gene expression in cultured mammalian cells. Here, we utilize a novel method that uses the reactivation of an X-inactivated GFP transgene as a marker to enrich for cells that have undergone drug-induced demethylation. By combining it with microarray gene expression profiling, we demonstrate the method’s utility in identifying genes activated by global DNA demethylation. Keywords: 5-aza-2'-deoxycytidine; methylation; dermal fibroblast; X-linked GFP

2006-04-27 | GSE4718 | GEO

Expression data from paediatric ependymoma short-term cell cultures

Project description:Promoter hypermethylation and transcriptional silencing is a common epigenetic mechanism of tumour suppressor inactivation in cancer, including malignant brain tumours. To identify targets of epigenetic silencing mediated by CpG island methylation in paediatric ependymoma, we used a pharmacological unmasking approach through treatment with the demethylating agent 5-Aza-2M-bM-^@M-^Y-deoxycytidine followed by global expression microarray analysis. Three short-term ependymoma cell cultures were used for whole genome expression analysis following treatment with the demethylating agent 5-Aza-dC (5 M-BM-5mol/L) or mock-treated with DMSO (M-bM-^IM-$0.1% v/v) for 96-hrs.

2013-12-02 | E-GEOD-45437 | biostudies-arrayexpress

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