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

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

PROVIDER: PRJNA750118 | ENA |

REPOSITORIES: ENA

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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

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 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

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

2011-08-18 | GSE31441 | GEO

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

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

| PRJNA749038 | ENA

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.

2010-10-07 | E-GEOD-18454 | biostudies-arrayexpress

Gene expression changes following demethylation by 5-aza-2'-deoxycytidine in primary mouse dermal fibroblasts

Project description:DNA methylation can contribute to the stable transcriptional silencing of mammalian genes. Oftentimes, these genes are important developmental regulators, and their silencing in cell types where they are not supposed to be active is important for the phenotypic stability of the cells. To identify key developmental regulator genes whose expression in terminally differentiated cells may be inhibited by DNA methylation, mouse dermal fibroblasts were demethylated with 5-aza-2’-deoxycytidine, and changes in gene expression monitored by microarray analysis. Keywords: 5-aza-2'-deoxycytidine; methylation; dermal fibroblast

2006-04-25 | GSE4696 | GEO

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.

2015-08-25 | GSE72295 | GEO

SUMO pulldown proteomics Namalwa 5-Aza-2' deoxycytidine treatment

Project description:Combination therapies targeting malignancies aim to increase treatment efficacy and reduce toxicity. Hypomethylating drug 5-Aza-2’-deoxycytidine (5-Aza-2’) enhances transcription of tumor suppressor genes and induces replication errors via entrapment of DNMT1. Post-translational modification by SUMO plays major roles in the DNA damage response and is required for degradation of entrapped DNMT1. Here, we combine SUMOylation inhibitor TAK981 and DNA-hypomethylating agent 5-Aza-2’ to improve treatment of MYC driven hematopoietic malignancies, since MYC overexpressing tumors are sensitive to SUMOylation inhibition. We studied the classical MYC driven malignancy Burkitt lymphoma, as well as diffuse large B-cell lymphoma (DLBCL) with and without MYC translocation. SUMO inhibition prolonged the entrapment of DNMT1 to DNA, resulting in DNA damage. An increase in DNA damage was observed in cells co-treated with TAK981 and 5-Aza-2’. Both drugs synergized to reduce cell proliferation in vitro in a B cell lymphoma cell panel, including Burkitt lymphoma and DLBCL. In vivo experiments combining TAK981 (25 mg/kg) and 5-Aza-2’ (2.5 mg/kg) showed a significant reduction in outgrowth of Burkitt lymphoma in an orthotopic xenograft model. In contrast, single dosing of TAK981 was ineffective and single dosing of 5-Aza-2’ only led to a modest outgrowth reduction. TAK981 and 5-Aza-2’ synergize to reduce B cell Lymphoma outgrowth in vitro and in vivo. SUMOylation is a key-player in the repair of DNA damage, hence upon TAK981 treatment the repair of DNA damage induced by 5-Aza-2’ treatment is impaired. Our results demonstrate the potential of tailored combination of drugs, based on insight in molecular mechanisms, to improve the efficacy of cancer therapies.

2023-03-17 | PXD038620 | Pride

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