Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA95245 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This microarray dataset accompanies the publication by Kim et al, "The retinoic acid synthesis gene ALDH1a2 is a candidate tumor suppressor in prostate cancer". The dataset comprises four prostate cancer cell lines treated with the DNA methyltransferase inhibitor 5-aza-dC. For each cell line, gene expression in treated (channel 2; Cy5) and untreated (channel 1; Cy3) cells is directly compared by hybridization to the same DNA microarray. Further details on the treatment conditions are provided in the manuscript.
2005-10-18 | E-SMDB-3416 | biostudies-arrayexpress
Project description:This microarray dataset accompanies the publication by Kim et al, "The retinoic acid synthesis gene ALDH1a2 is a candidate tumor suppressor in prostate cancer". The dataset comprises four prostate cancer cell lines treated with the DNA methyltransferase inhibitor 5-aza-dC. For each cell line, gene expression in treated (channel 2; Cy5) and untreated (channel 1; Cy3) cells is directly compared by hybridization to the same DNA microarray. Further details on the treatment conditions are provided in the manuscript. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Using regression correlation
2010-07-01 | E-GEOD-2932 | biostudies-arrayexpress
Project description:This microarray dataset accompanies the publication by Kim et al, "The retinoic acid synthesis gene ALDH1a2 is a candidate tumor suppressor in prostate cancer". The dataset comprises four prostate cancer cell lines treated with the DNA methyltransferase inhibitor 5-aza-dC. For each cell line, gene expression in treated (channel 2; Cy5) and untreated (channel 1; Cy3) cells is directly compared by hybridization to the same DNA microarray. Further details on the treatment conditions are provided in the manuscript. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design
2006-01-25 | GSE4089 | GEO
Project description:This microarray dataset accompanies the publication by Kim et al, "The retinoic acid synthesis gene ALDH1a2 is a candidate tumor suppressor in prostate cancer". The dataset comprises four prostate cancer cell lines treated with the DNA methyltransferase inhibitor 5-aza-dC. For each cell line, gene expression in treated (channel 2; Cy5) and untreated (channel 1; Cy3) cells is directly compared by hybridization to the same DNA microarray. Further details on the treatment conditions are provided in the manuscript. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Keywords: compound_treatment_design
2006-05-08 | GSE2932 | GEO
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
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. Reduced representation bisulfite sequencing (MspI,~40-220bp size fraction) of murine and human cells.
2015-08-25 | E-GEOD-72295 | biostudies-arrayexpress
Project description:Purpose: The major aim of this study was to investigate the role of DNA methylation (referred to as methylation) on microRNA (miRNA) silencing in non-small cell lung cancers (NSCLC). Experimental Design: We performed microarray expression analyses of 856 miRNAs in NSCLC A549 cells before and after treatment with the DNA methyltransferase inhibitor 5-aza-2´-deoxycytidine (Aza-dC) and with a combination of Aza-dC and the histone deacetylase inhibitor trichostatin A. MiRNA methylation was determined in 11 NSCLC cell lines and in primary tumors and corresponding non-malignant lung tissue samples of 101 stage I-III NSCLC patients. Results: By comparing microarray data of untreated and drug treated A549 cells, we identified 33 miRNAs whose expression was upregulated after drug treatment and which are associated with a CpG island. Thirty (91%) of these miRNAs were found to be methylated in at least 1 of 11 NSCLC cell lines analysed. Moreover, miR-9-3 and miR-193a were found to be tumor-specifically methylated in NSCLC patients. We observed a shorter disease-free survival of miR-9-3 methylated lung squamous cell carcinoma (LSCC) patients compared to miR-9-3 unmethylated LSCC patients by multivariate analysis (HR = 3.8, 95% CI = 1.3 to 11.2, p = 0.017) and a shorter overall survival of miR-9-3 methylated LSCC patients compared to miR-9-3 unmethylated LSCC patients by univariate analysis (p = 0.013). Conclusions: Overall, our results suggest that methylation is an important mechanism for inactivation of certain miRNAs in NSCLCs and that miR-9-3 methylation may serve as a prognostic parameter in LSCC patients. MiRNA expression (LC Sciences, mirBASE12) was analyzed before and after treatment of A549 cells with 5-aza-2´-deoxycytidine (Aza-dC) and a combination of Aza-dC and trichostatin A (TSA). Experiments were performed in duplicates.
2012-03-13 | E-GEOD-31579 | biostudies-arrayexpress
Project description:Treatment-related DNA hypermethylation may play a role in creating drug resistant phenotypes by inactivating genes that are required for cytotoxicity, but there have been no genome-wide studies to systematically investigate methylation of individual genes following exposure to chemotherapy. We used microarrays and a pharmacologic unmasking protocol in isogenic cisplatin-sensitive and -resistant cell lines to identify genes that were down-regulated in cisplatin-resistant cells and could be re-activated by the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine (5-Aza-dC). We identified several hundred genes that were down-regulated in each resistant cell line. Of these, 30 genes were common to > 2 cell lines, and/or reported to be down-regulated in previous studies. siRNA knockdown of two candidate genes increased cell viability with cisplatin treatment in sensitive parental cell lines Cisplatin-sensitive and -resistant SCC cells and KB and KB cisplatin-resistant clones (n=2) were split to low density and treated with freshly prepared 5 microM 5-Aza-dC dissolved in 50% acetic acid/50% PBS or were mock treated with the same volume of vehicle in the media for 5 days. Subsequently, RNA was extracted and hybridized on Affymetrix U133A microarrays. Signal intensity and statistical significance was established for each transcript, and a 2-fold decrease in signal in each paired sensitive/resistant cell line in combination with 1.5-fold increase after 5Aza-dC treatment was used to identify candidate genes.
2010-04-12 | E-GEOD-19397 | biostudies-arrayexpress
Project description:To genome-wide screening for the genes whose expression are responsible for the promoter DNA methylation, we performed the cDNA microarray with oral cancer cells before and after a DNA methyltransferase inhibitor, 5-aza-2’-deoxycytidine (AzC), treatment. Total RNA was collected from four oral cancer cell lines before or after AzC treatment.
2015-04-01 | E-GEOD-38823 | biostudies-arrayexpress
Project description:Myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) are diseases of abnormal hematopoietic differentiation with aberrant epigenetic alterations. Azacitidine (AZA) is a DNA methyltransferase inhibitor (DNMTi) widely used to treat MDS and AML, yet the impact of AZA on the cell surface proteome has not been defined. To identify potential therapeutic targets for use in combination with AZA in AML patients, we investigated the effects of AZA treatment on four AML cell lines representing different stages of differentiation. The effect of AZA treatment on these cell lines was characterized at three levels: the DNA methylome, the transcriptome, and the cell surface proteome. Untreated AML cell lines showed substantial overlap at all three omics level; however, while AZA treatment globally reduced DNA methylation in all cell lines, changes in the transcriptome and surface proteome were subtle and differed among the cell lines. Transcriptome analysis identified five commonly up-regulated coding genes upon AZA treatment in all four cell lines, TRPM4 being the only gene encoding a surface protein, and surface proteomics analysis found no commonly regulated proteins. Gene Set Enrichment Analysis (GSEA) of differentially-regulated RNA and surface proteins showed a decrease in metabolism pathways and an increase in immune defense response pathways. As such, AZA treatment led to diverse effects at the individual gene and protein level but converged to common responses at the pathway level. Given the heterogeneous responses in the four cell lines, we discuss potential therapeutic strategies for AML in combinations with AZA.
2018-10-07 | MSV000083006 | MassIVE