Project description:To evaluate the impact of DNA demethylating agents on our mouse MDS model, we chose 5-aza-2’-deoxycytidine, decitabine (DAC), one of the DNA demethylating agents, which is incorporated into DNA but not RNA and has 10-fold more potency in DNA demethylation than 5-azacitidine. We transplanted Tet2KD/KDEzh2Δ/Δ MDS cells into lethally irradiated secondary recipients and treated them with DAC (low dose DAC at 0.25mg/kg, 3 times a week, intraperitoneal injection), then purified LSK HSPCs and evaluated the expression profiles.
Project description:Our study had shown that DAC treatment enhanced immunogenecity of EL4 cells. To explore the mechanisms of DAC-induced tumor immunity, we carried out cDNA microarray analyses to compare the differential expression of genes between DAC and PBS treated EL4 cells. Two-condition experiment, PBS treated EL4 vs. Decitabine treated EL4 cells. Biological replicates: 3 PBS treated, 3 Decitabine treated, independently treatment and harvested. One replicate per array.
Project description:To analyze the differential miRNA expression profiling in human lymphoma cells (Namalwa cell line) before and after treatment by DNA methylation inhibitor 5-aza-2'-deoxycytidine (Decitabine; 5-aza).
Project description:Epigenetic changes in DNA methylation are involved in periodontitis pathogenesis and recent studies indicate that DNA methyltransferase (DNMT) inhibitors may protect against bone resorption and disruption of the epithelial barrier. To assess the impact of DNMT inhibition on gingival fibroblasts (GFs), cells were cultured with decitabine (5-aza-2’-deoxycytidine, DAC) for 12 days to induce DNA hypomethylation. Analysis of DAC-induced genes in resting or P. gingivalis-infected GFs identified by RNA sequencing revealed increased expression of CCL20, CCL5, CCL8, CCL13, TNF, IL1A, IL18, IL33, and CSF3, and showed that the most affected processes were related to immune and inflammatory responses. In contrast, the genes downregulated by DAC were associated with extracellular matrix and collagen fibril organization.
Project description:To analyze the differential miRNA expression profiling in human lymphoma cells (Namalwa cell line) before and after treatment by DNA methylation inhibitor 5-aza-2'-deoxycytidine (Decitabine; 5-aza). Six total samples were analyzed, two groups, and triplicate for each group. The abbreviation of Con represents Namalwa cells without the treatment of 5-aza, and Add represents Namalwa cells after treatment by 5-aza for 3 days.
Project description:5-Azacytidine (Aza) and 5-Aza-2'-deoxycytidine (Dac) are the only epigenome modifying drugs in widespread clinical use, and are some of the primary therapeutics for Acute Myeloid Leukaemia treatment. The two are frequently used interchangeably, surprisingly as their selectivity of de-methylation is unique from the other, with to date no identified predictors of response or known biomarkers to indicate drug preference. Using these drugs to induce de-methylating conditions, we combine data from DRIPc-Seq, Immunostaining, RNA-Seq and Mass spectrometry with epigenetic analysis to uncover unique cellular responses following Aza and Dac treatment.
Project description:5-Azacytidine (Aza) and 5-Aza-2'-deoxycytidine (Dac) are the only epigenome modifying drugs in widespread clinical use, and are some of the primary therapeutics for Acute Myeloid Leukaemia treatment. The two are frequently used interchangeably, surprisingly as their selectivity of de-methylation is unique from the other, with to date no identified predictors of response or known biomarkers to indicate drug preference. Using these drugs to induce de-methylating conditions, we combine data from DRIPc-Seq, Immunostaining, RNA-Seq and Mass spectrometry with epigenetic analysis to uncover unique cellular responses following Aza and Dac treatment.
Project description:5-Azacytidine (Aza) and 5-Aza-2'-deoxycytidine (Dac) are the only epigenome modifying drugs in widespread clinical use, and are some of the primary therapeutics for Acute Myeloid Leukaemia treatment. The two are frequently used interchangeably, surprisingly as their selectivity of de-methylation is unique from the other, with to date no identified predictors of response or known biomarkers to indicate drug preference. Using these drugs to induce de-methylating conditions, we combine data from DRIPc-Seq, Immunostaining, RNA-Seq and Mass spectrometry with epigenetic analysis to uncover unique cellular responses following Aza and Dac treatment.
