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

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

PROVIDER: PRJNA749038 | ENA |

REPOSITORIES: ENA

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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.

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MCF7 cells gene expression change by inducing CpG demethylation using 5-Aza-2'-deoxycytidine (Aza)

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MCF7 cells gene expression change by inducing CpG demethylation using 5-Aza-2'-deoxycytidine (Aza)

Project description:Promoter methylation is able to induce downregulation of gene expression. 5-Aza-2'-deoxycytidine(Aza), methytransferase inhibitor, induce CpG demethylation. Here, 5-Aza-2'-deoxycytidine(Aza) is treated in a human breast cancer cell, MCF7, for detection of gene expression change. To analyze gene expression change by aza, control RNA isolated from MCF-7 was compared with RNA isolated from MCF-7 treated with 5uM and 10uM aza.

2011-08-17 | E-GEOD-31441 | biostudies-arrayexpress

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

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Analysis of normal lung cells treated with 5-aza-dC to induce DNA demethylation

Project description:Analysis of 2 cultured normal lung cell lines, Normal Human Bronchial Epithelial (NHBE) and Human Small Airway Epithelial (SAEC) cells (Lonza, Walkersville, MD), following treatment with 5-aza-dC to induce DNA demethylation. These results provide insight into the role of epigenetic alterations, specifically demethylation, in differential gene expression in various lung neoplasms. Two normal lung cell lines, NHBE and SAEC, were treated with 5uM 5-aza deoxycytidine for 72 hours and Trichostatin A for 24 hours prior to harvesting total RNA for expression array analysis using the Affymetrix Human Genome U133 Plus 2.0 expression platform. Signal intensity and statistical significance was established for each transcript using dChip version 2005. Two-fold increase based on the 90% confidence interval of the result and expression minus baseline >50 was used as the statistical cutoff value after 5Aza-dC and/or TSA treatment to identify upregulated candidate genes.

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5-aza-2-deoxycytidine treatment of Swarm rat chondrosarcoma cells

Project description:The puropose of this experiment was to identify gene expression changes that result from 5-aza-2-deoxycytidine induced DNA demethylation of Swarm rat chondrosarcoma cells. The gene expression profiles of untreated Swarm rat chondrosarcoma cells were compared to the gene expression profiles of Swarm rat chondrosarcoma cells that were treated for 5 passages with a low dose of 5-aza-2-deoxycytidine (0.1uM).

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A high-throughput screen of inactive X chromosome reactivation identifies the enhancement of DNA demethylation by 5-aza-2’-dC upon inhibition of ribonucleotide reductase-wide

Project description:Background: DNA methylation is important for maintenance of the silent state of genes on the inactive X chromosome (Xi). Here, we screened for siRNAs and chemicals that reactivate an Xi-linked reporter in the presence of 5-aza-2’-deoxycytidine (5-aza-2’-dC), an inhibitor of DNA methyltransferase 1, at a concentration that, on its own, is not sufficient for Xi-reactivation. Results: We found that inhibition of ribonucleotide reductase (RNR) induced expression of the reporter. RNR inhibition potentiated the effect of 5-aza-2’-dC by enhancing its DNA incorporation, thereby decreasing genome-wide DNA methylation levels. Since both 5-aza-2’-dC and RNR-inhibitors are used in the treatment of hematological malignancies, we treated myeloid leukemia cell lines with 5-aza-2’-dC and the RNR inhibitor hydroxyurea, and observed synergistic inhibition of cell growth and decreases in genome-wide DNA methylation. Conclusions: Taken together, our study identifies a drug combination that enhances DNA demethylation by altering nucleotide metabolism. We demonstrate that XCR assays can be used to optimize epigenetic activity of drug combinations.

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Analysis of normal lung cells treated with 5-aza-dC to induce DNA demethylation

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