Aza treated AML3 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Peter Adams
PROVIDER: E-GEOD-55125 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:AML3 cells were treated with Azacytidine and compared against untreated cells Examination of methylation status in human untreated and Azacytidine treated AML3 cells
2014-07-01 | E-GEOD-55124 | biostudies-arrayexpress
Project description:AML3 cells were treated with Azacytidine and compared against untreated cells We used RNA-Seq to detail the global programme of gene expression in human untreated and Azacytidine treated AML3 cells
2014-07-01 | E-GEOD-55123 | biostudies-arrayexpress
Project description:DNA double strand breaks (DSBs) are a major source of mutations. Both non-homologous-end-joining (NHEJ) and microhomology-mediated-end-joining (MMEJ) DSB repair pathways are error prone and produce deletions, which can lead to cancer. DSBs also lead to epigenetic changes, including demethylation, which is involved in carcinogenesis. Of specific interest is the MMEJ repair pathway, as it requires methylation restoration around the break, as a result of the resection and formation of single stranded (ssDNA) intermediates. While, methylation patterns after homologous recombination (HR) have been partially studied, the methylation status after MMEJ and NHEJ remains poorly reported, and can be relevant for cancer. To study methylation patterns around DSB after NHEJ and MMEJ repair, we used targeted bisulfite-sequencing (BS-seq) to quantify methylation of dozens of single cell clones after induction of DSB by CRISPR. Each single cell clone was classified according to the sequence signature to a specific repair mechanism: NHEJ or MMEJ. Comparison of single cell clones after DSB to control cells, without DSB, demonstrated correct restoration of the methylation levels. No difference in methylation patterns was noticed when comparing NHEJ to MMEJ. Methylation levels in gene body, highly methylated CpGs (n=61, 4000 base pairs around DSB) and in low methylation CpGs (n=19), remained stable after both MMEJ and NHEJ. Gene body methylation persisted even on the background of DNMT3A R882C mutation, the most prevalent preleukemic mutation, in which the de novo methylation machinery is compromised. An exception observed in a single CpG site (ASXL1 995) which demonstrated elevated methylation rate after DSB repair only in the presence of WT DNMT3A. In summary, DNA methylation restoration demonstrated high fidelity after DSB both in methylated and unmethylated gene body, even in cases where DNA resections and deletions occurred.
2022-08-25 | E-MTAB-12061 | biostudies-arrayexpress
Project description:Human acute myeloid leukemia cell lines OCI-AML2 and OCI-AML3 were used in a CRISPR/Cas9-mediated approach to specifically target DDX3X’s gene sequences encoding the RNA binding domain of the helicase. DDX3X RNA binding domain is bipartite in the two halves of the helicase core. sgRNAs were designed to target both halves of the domain (named RNA binding domain A and B – RBDA and RBDB). We performed RNA-seq to observe the gene expression changes in both OCI-AML2 and OCI-AML3 cell lines following the not-combined CRISPR/Cas9 –mediated targeting of both regions of the DDX3X RNA binding domain. Control CRISPR/Cas9 performed with no sgRNA expressing vector (named “empty vector”) was performed in both cell lines. The latter condition was used as a control for gene expression changes analysis, for each cell line.
2019-11-23 | E-MTAB-6241 | biostudies-arrayexpress
Project description:MicroRNAs (miRs) are small non-coding RNAs that can function as tumor suppressor genes. We previously reported that miR-1 is among the most consistently down-regulated miRs in primary human prostate tumors. In this follow-up study, we further corroborated this finding in an independent dataset and made the novel observation that miR-1 expression is further reduced in distant metastasis and is a predictor of disease recurrence. Moreover, we performed in vitro experiments to explore the candidate tumor suppressor function of miR-1. Cell-based assays showed that miR-1 is epigenetically silenced in human prostate cancer cells. Overexpression of miR-1 in these cells led to growth inhibition and down-regulation of genes in pathways regulating cell cycle progression, mitosis, DNA replication/repair, and actin dynamics. This observation was further corroborated with protein expression analysis and 3’-UTR-based reporter assays, indicating that genes in these pathways are either direct or indirect targets of miR-1. A gene set enrichment analysis revealed that miR-1-mediated tumor suppressor effects are globally similar to those of histone deacetylase inhibitors. Lastly, we obtained preliminary evidence that miR-1 alters gH2A.X marker expression and affects the cellular organization of F-actin and filipodia formation. In conclusion, our findings indicate that miR-1 acts as a tumor suppressor in prostate cancer by influencing multiple cancer-related processes and by inhibiting cell proliferation and motility. In this study we monitored global miRNA expression changes in prostate cancer LNCaP cells treated with the epigenetic compounds 5-Azacytidine (5-AzaC) and/or trichostatin A (TSA). Cells were treated with epigenetic drugs for 36 hours and total RNA was isolated for hybridization to miRNA microarrays. 5 independent experiments were performed (n=4 for combined treatment). The candidate prostate tumor suppressor miRNAs, miR-1, miR-206, and miR-27 were up-regulated in LNCaP cells for Affymetrix microarray analysis. LNCaP cells were transfected with pre-miR oligos and 24 hr post-transfection total RNA was collected for microarray analysis; total of three independent experiments.
2011-12-01 | E-GEOD-31620 | biostudies-arrayexpress
Project description:The nucleolar scaffold protein NPM1 acts as a multifunctional regulator of cellular homeostasis, genome integrity, and stress response. NPM1 mutations, known as NPM1c variants that promote its aberrant cytoplasmic localization, are the most frequent genetic alterations in acute myeloid leukemia (AML). A hallmark of AML cells is their dependency on elevated autophagic flux. In order to identify the proteome changes upon NPM1 and NPM1c overexpression, we performed TMT-labeled mass spectrometry analysis of whole cell lysates.
2023-10-28 | PXD045357 | Pride
Project description:Glucocorticoids induce rapid apoptosis of rat primary thymocytes through mechanisms requiring altered gene expression. The determination of genes regulating glucocorticoid-induced apoptosis of lymphocytes has received considerable attention. However, the role of specific non-coding microRNAs in the regulation of glucocorticoid-induced apoptosis of lymphocytes is poorly defined. Using deep sequencing analysis, we have identified microRNAs differentially expressed during glucocorticoid-induced apoptosis of rat primary thymocytes. We have also identified numerous loci that harbor probable novel microRNAs. Furthermore, we have validated the glucocorticoid-responsive expression of 2 novel microRNAs in the apoptotic rat primary thymocyte. These 2 novel microRNAs are predicted to target numerous messenger RNAs throughout the genome. Using whole genome expression analysis, we now seek to correlate the altered expression of these novel microRNAs with the expression of their predicted target mRNAs during glucocorticoid-induced apoptosis. Changes in gene expression during glucocorticoid-induced apoptosis of rat primary thymocyes (3 biological replicates) were measured after 6 hours of 100nM dexamethasone treatment in-vitro.
2014-03-26 | E-GEOD-45560 | biostudies-arrayexpress
Project description:AZD4547,pan-FGFR inhibitor, have been reported to have profound therapeutic effects on FGFR-deregulated cancers. AN3-CA is one of endometrial cancer cell lines harbouring FGFR2 mutants. AZD4547 showed a potent antiprolierative effect on AN3-CA cells. we used microarray to investigate transcriptome-wide change in gene expression followinig 300 nM AZD4547 treatment to explain the chemotherapeutic effect. compound treatment with or without ligand stimulus.
2015-09-17 | E-GEOD-61481 | biostudies-arrayexpress
Project description:Mammary gland development and luminal differentiation occur largely postnatally during puberty and pregnancy. To explore the role of DNA methylation in luminal cell differentiation and pregnancy-induced changes, we determined the genome-wide DNA methylation and gene expression profiles of mammary epithelial stem, luminal progenitor, and mature luminal cells at different reproductive stages. We found that pregnancy had the most significant effects on stem cells, inducing a distinct epigenetic state that remained stable through life. Integrated analysis of gene expression, DNA methylation, and histone modification profiles revealed cell type and reproductive stage-specific changes in molecular signatures. We also identified p27 and TGFβ signaling as key regulators of luminal progenitor cell proliferation based on their expression patterns and by the use of explant cultures. Our results suggest relatively minor changes in DNA methylation during luminal cell differentiation as compared to the significant effects of pregnancy on mammary epithelial stem cells. Mammary glands were collected from mice treated with DNA methylation inhibitor 5-azacytidine (AzaC) and histone deacetylase inhibitor valproic acid (VPA) at non-pregnant and pregnant stages for RNA extraction and hybridization on Affymetrix microarrays.
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Project description:Effects of supernatants from four strains of Pseudomonas aeruginosa on global gene expression in Candida albicans
2008-11-12 | E-MEXP-1614 | biostudies-arrayexpress