DAC: RNAseq Iron-Treated iPSC-derived Microglia
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ABSTRACT:
PROVIDER: EGAC00001002605 | EGA |
REPOSITORIES: EGA
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Project description:To globally evaluate to what extend the p53 mutant transcription activity can be restored by arsenic trioxide (ATO) and decitabine (DAC) co-treatment, p53-null THP-1 cells introduced with p53-R282W or wild-type p53 were treated with ATO (1 μg/ml) and DAC (5 μM). mRNA was isolated and then subject to deep sequencing, using Illumina HiSeq. The sequence reads that passed quality filters were analyzed using Cutadapt.
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Project description:DAC-treated tumor tissue from PDX model and DAC-treated CT26 cells.
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Project description:To identify genes responsible for the synergistic effect of DAC with Dex, we performed cDNA microarray analyses using cDNA prepared from Dex-resistant OPM1 cells treated with/without Dex, DAC or DAC+Dex.
2009-01-03 | GSE14261 | GEO
Project description:We observed gene expression difference between different groups after MDA-MB-231 treated with DMSO, 10 μM DAC, 1 μM DEX, or DAC+DEX. Data obtained from high-throughput sequencing (Illumina NovaSeq 6000 platform) were transformed into raw sequenced reads by CASAVA base calling and stored in FASTQ format. Gene expression of each groups are listed in raw data files. Some different expression genes between two groups are further validated with qRT-PCR.
2023-05-09 | GSE175867 | GEO
Project description:Epigenetic reprogramming using demethylating drugs is a promising approach for cancer therapy, but its efficacy is highly dependent on the dosing regimen. Low-dose treatment for a prolonged period shows a high therapeutic efficacy, despite its small demethylating effect. Here, we aimed to reveal the mechanisms of how such low-dose treatment shows high efficacy by focusing on epigenetic reprograming at the single-cell level. Single-cell RNA-sequencing of HCT116 cells treated with decitabine (DAC) revealed that up-regulated genes were highly variable at the single-cell level. To analyze functional consequences at the single-cell level, DAC-treated HCT116 cells were cloned. While only partial reduction of methylation levels was observed in bulk cells, complete demethylation of specific cancer-related genes was observed, depending upon clones. For example, p16 was completely demethylated in the H3-32 clone out of 9 clones, and this clone showed slower proliferation than other clones without demethylation. In addition, in this clone, the fraction of cells with tetraploid became much larger, indicating that cellular senescence was induced. These results showed that epigenetic reprogramming of specific cancer-related pathways at the single-cell level is likely to underlie the high efficacy of low-dose DNA demethylating therapy.
2021-04-10 | GSE171429 | GEO
Project description:Reversal of gene promoter DNA hypermethylation and associated abnormal gene silencing is an attractive approach to cancer therapy. The DNA methylation inhibitor, decitabine (5-aza-2'-deoxycitidine), is proving efficacious for hematological neoplasms especially at lower, less toxic, doses. Experimentally, high doses induce rapid DNA damage and cytotoxicity, but these may not explain the prolonged time to response seen in patients. Transient exposure of leukemic and solid tumor cells to clinically-relevant nanomolar doses, without causing immediate cytotoxicity or apoptosis, produces sustained reduced tumorigenicity, and for leukemia cells, diminished long-term self-renewal. These effects appear triggered by cellular reprogramming and include sustained decreases in promoter DNA methylation with associated gene re-expression, and anti-tumor changes in multiple key cellular regulatory pathways, most of which are high priority targets for pharmacologic anti-cancer strategies. Thus, low dose decitabine regimens appear to have broad applicability for cancer management. [Gene expression profiling] Leukemia cell lines Kasumi-1 and KG1A are treated with 10nM DAC during 72 hours and gene expression was assayed at day 3, 7 and 14 after the start of the treatment. Appropriate mock treated samples were used as control in each case. In addition, Kasumi-1 cells were also treated with a higher dose of DAC (500nM), 100nM ARA-C and 300 nM TSA, again controlled against mock treated Kasumi-1 cells, to separate dose and agent dependent effects. MCF7 was studied as an example of a solid tumor cell line. Therefore MCF7 cells were treated with 100nM DAC and results were assayed at day 1, day 3 and day 10. [Methylation profiling] The effects of the demethylating agent DAC were studied in the leukemia cell line Kasumi-1 over a 28 day time course. Intermediate time points were studied at days 3, 7, 14 and 21. These results were verfied in KG1A and KG1 leukemia cell lines, at one selected time point. The effects on one primary sample were also studied. Four normal leukemia samples (PL1, 2, 4 and 5) were used as general controls. The effect of DAC was compared to ARA-C, TSA. Both mock treated and day 3 DAC treated Kasumi-1 cells were repeated. These results were verified at one selected time point for the DAC treated MCF7 breast cancer cell line.
2012-03-21 | E-GEOD-20945 | biostudies-arrayexpress
Project description:Aberrant expression of microRNA (miRNA) has been reported in various cancers. To clarify the role of miRNA in gastric carcinogenesis, we performed miRNA microarray analysis and investigated expressional changes of miRNAs in a 5-aza-2'-deoxycytidine (DAC)-treated gastric cancer cell line, KATO-ІІІ.
2010-01-20 | GSE16006 | GEO
Project description:DAC represents a therapeutic option for elderly AML patients. However, there is still a lack of data for valid biomarkers in respect to response. We executed a gene expression analysis prior to treatment to evaluate gene expression patterns associated with response that might be used to predict DAC therapy outcome. In our cohort an objective ORR of 27% was seen. In a class comparison analysis 333 genes were identified that correlated significantly with response. In this gene signature genes that were prior associated with adverse outcome to regular chemotherapy were enriched in the response group. Interistingly for the non response cohort TSG showed an increased expression, suggesting that epigenetic silencing due to promoter hypermethylation might play a lesser role in theses leukemia pathogenesis.
2016-12-31 | GSE84334 | GEO
Project description:8 neuroblastoma (NB) cell lines (CLB-GA, IMR-32, SH-SY5Y, N206, CHP-902R, LAN-2, SK-N-AS, SJNB-1) were profiled on the Affymetrix HGU-133plus2,0 platform before and after treatment with DAC (2'-deoxy-5-azacytidine) to investigate the influence on expression after inhibiting DNA-methylation 8 NB cell lines were included (CLB-GA, IMR-32, SH-SY5Y, N206, CHP-902R, LAN-2, SK-N-AS, SJNB-1), before and after treatment with 3 micromolars of DAC for 3 days
2012-09-13 | E-GEOD-31229 | biostudies-arrayexpress
Project description:We found frequent epigenetic silencing of microRNA-34b/c in human colorectal cancer. Introduction of miR-34b/c into a colorectal cancer cell line induced significant changes in gene expression profile. We also found overlap between the genes downregulated by miR-34b/c and those downregulated by DAC. Keywords: dose response A colorecal cancer cell line HCT116 was transfected with miR-34b or -c precursor or negative control. Also, HCT116 was treated with 5-aza-2'-deoxycytidine (DAC) or mock. Genes up- or downregulated by miR-34b/c and those by DAC was compared.
2008-04-30 | E-GEOD-10455 | biostudies-arrayexpress