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.
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.
Project description:CpG hypermethylation in gene promoters is a frequent mechanism of tumor suppressor gene silencing in various types of cancers. 5-aza-2'-deoxycytidine (AZA) is a DNA demethylating and anti-cancer agent resulting in induction of genes suppressed via DNA hypermethylation. Using microarray expression profiling of AZA or DMSO treated and untreated breast cancer (MCF7 and MDA-MB-231) and non-tumorigenic breast (NTB) cells, we aim to identify candidate genes that are downregulated via promoter hypermethylation in breast cancer.
Project description:Ornithine decarboxylase antizyme 1 mediates DNA demethylation. Using a human oral cancer cell line, UM1, genes induiced by DNA demethylation were screened. To verify the methylation status of those induced genes, the gene expression profile was compared with that of 5-Aza-2’-deoxycytidine treated sample. Keywords: DNA demthylation, ornithine decarboxylase antizyme 1, 5-Aza-2’-deoxycytidine
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
Project description:The goal of this study is to identify the DNA methylation changes caused by exposure of to the DNMT inhibitor 5-aza-2â-deoxycytidine (5Aza) and HDAC inhibitor Trichostatin A (TSA). We performed whole-genome bisulfite sequencing of the drug-treated MCF7 breast cancer cell lines and compare their DNA methylation profile with the untreated MCF7 (see E-MTAB-2014). While MCF7 treated with both drugs experienced global loss of DNA methylation, the 5Aza induced stronger demethylation than TSA.
Project description:The goal of this study is to identify the gene expression changes caused by exposure of to the DNMT inhibitor 5-aza-2'-deoxycytidine (5Aza) and HDAC inhibitor Trichostatin A (TSA). We performed rRNA-depleted RNA sequencing of the untreated and drug-treated MCF7 breast cancer cell lines and carried out differential gene expression analysis. Although 5Aza caused a stranger demethylation effect than TSA, there were fewer differentially expressed gene in the 5Aza-treated MCF7 than the TSA-treated cells.
Project description:Ornithine decarboxylase antizyme 1 mediates DNA demethylation. Using a human oral cancer cell line, UM1, genes induiced by DNA demethylation were screened. To verify the methylation status of those induced genes, the gene expression profile was compared with that of 5-Aza-2â-deoxycytidine treated sample. Preparation of samples, hybridization process and data analysis were performed according to the manufacture's protocol (BD Biosciences). To verify the genes induced by ornithine decarboxylase antizyme via DNA demethylation, 5-Aza-2â-deoxycytidine treatment was carried out as a parallel experiment.
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).
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). Five chip study. For these experiments, microarray was carried out on untreated (control) Swarm rat chondrosarcoma cells (3 biological replicates), and microarray was also carried out on Swarm rat chondrosarcoma cells treated with 5-aza-2-deoxycytidine (2 biological replicates).