Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

31 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Histone deacetylases positively regulate transcription through the elongation machinery

ABSTRACT: Global run-on sequencing (GRO-seq) analysis of breast cancer cells upon perturbations of transcription elongation regulators.

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Homo sapiens

SUBMITTER: Tae Hoon Kim

PROVIDER: E-MTAB-3626 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq with metabolic labelling of human lymphoblast cell line K562 treated with a panel of 83 different epigenetically active compounds and untreated controls

Project description:This experiment has utilized metabolic labeling coupled with RNA-sequencing to identify directly responding genes after perturbing cellular enzymes affecting epigenetic modifications.

2024-01-01 | E-MTAB-13091 | biostudies-arrayexpress

Histone deacetylases positively regulate transcription through the elongation machinery

Project description:Chromatin immunoprecipitation sequencing (ChIP-seq) analysis of elongation factors in breast cancer cells upon HDAC inhibition.

2015-10-20 | E-MTAB-3631 | biostudies-arrayexpress

A Multi-loop, Double-cube Microarray Design Applied to Prostate Cancer Cell Lines with Variable Sensitivity to Histone Deacetylase Inhibitors

Project description:Implementation of a complex design for a microarray experiment on resistance mechanisms of histone deacetylase inhibitors (HDACI). To improve our understanding of the underlying mechanism of HDACI resistance in prostate cancer cells, we designed a novel ‘‘multiple-loop, double-cube’’ cDNA microarray experiment. In the experiment DU-145 and PC3 cells were treated with two different HDACIs (vorinostat and valproic acid) and incubation periods (48 and 96 hours). Preprocessing included exploratory analyses of the quality of the arrays and intensity-dependent within-array Loess normalization. An ANOVA model was used for inference. The results were validated by Western blot analysis of known treatment targets.

2011-12-17 | E-GEOD-34452 | biostudies-arrayexpress

Gene expression profiling of histone deacetylase inhibition in epithelioid sarcoma

Project description:Epithelioid Sarcoma (ES) is a rare neoplasm uniquely comprised of cells exhibiting both mesenchymal and epithelial features. Having propensity for local and distant recurrence, it can pose a diagnostic dilemma secondary to pathologic complexity. Patients have dismal prognosis due to lack of effective therapy. HDAC inhibitors exhibit marked anti-tumor effects in various malignancies. Our studies demonstrate that pan-HDAC inhibitors constitute potentially novel therapeutics versus ES. Human ES cells (VAESBJ, HS-ES, Epi544) were studied in vitro to evaluate the effects of HDACi. Gene array analysis was used to identify the impact of HDACi on ES gene expression in three cell lines.

2015-11-03 | E-GEOD-66800 | biostudies-arrayexpress

How basic nuclear processes are affected by selected HAT and HDAC inhibitors - Signalling pathways affected by HATs/HDACs inhibitor

Project description:Balance between histone acetylation and deacetylation is fundamental for proper gene function, thus knowledge of how to modulate these epigenetic processes is important for understanding of nuclear events, including replication, transcription, splicing and DNA repair. Here, we have studied an effect of HDAC inhibitor, SAHA, and we compared it with an effect of natural product, derivative of anacardic acid (MG149). Recently, it was discovered that MG149 has inhibitory potential for HATs' activity on histone H3 and H4 when tested on nuclear extracts.

2014-01-20 | E-MTAB-1481 | biostudies-arrayexpress

Gene expression profiling of drug-tolerant persister BT474 breast cancer cells derived from lapatinib treatment

Project description:Acquired drug resistance prevents targeted cancer therapy from achieving stable and complete responses. Emerging evidence implicates a key role for nonmutational mechanisms including changes in cell state during early stages of acquired drug resistance. Targeting nonmutational resistance may therefore present a therapeutic opportunity to eliminate residual surviving tumor cells and impede relapse. A variety of cancer cell lines harbor quiescent, reversibly drug-tolerant âpersisterâ cells which survive cytotoxic drugs including targeted therapies and chemotherapies. These persister cells survive drug through nonmutational mechanisms which are poorly understood. Specifically targeting persister cells is a promising strategy to prevent tumor relapse. We sought to identify therapeutically exploitable vulnerabilities in persister cells using the HER2-amplified breast cancer line BT474 as an experimental model. Similar to other persister cell models, upon treatment with the HER2 inhibitor lapatinib (2uM concentration) for nine or more days, the majority of BT474 cells die, revealing a small population of quiescent surviving persister cells. Removal of lapatinib allows the persister cells to regrow and to re-acquire sensitivity to lapatinib. Subsequent lapatinib treatment re-derives persister cells. The reversibility of persister cell drug resistance indicates a nonmutational resistance mechanism. Here we provide RNAseq gene expression profiling data generated from parental BT474 cells compared to BT474 persister cells generated from nine days of treatment with 2 uM lapatinib. These data can be used to identify genes and pathways which are upregulated in persister cells, revealing potential therapeutic targets. 3 biological replicates of BT474 persister cells, two biological replicates of BT474 parental cells

2016-07-28 | E-GEOD-84896 | biostudies-arrayexpress

HDAC1 and HDAC2 in fetal hemoglobin induction

Project description:This SuperSeries is composed of the following subset Series: GSE22366: Primary human erythroid progenitor cells HDAC1 and HDAC2 shRNA knockdown samples GSE22367: Primary human erythroid progenitor cells SAHA treatment samples GSE22368: Primary human erythroid progenitor cells NK57 treatment samples Refer to individual Series

2010-07-29 | E-GEOD-22369 | biostudies-arrayexpress

Expression profiling of HeLa cells at S and G2/M phases of mitotic cell cycle.

Project description:We compared the mRNAs expression profile of HeLa cells between two phases of the mitotic cell cycle: S and G2/M phases. Results provide insight into the regulation of transcript levels during mitotic cell cycle progression. HeLa cells were synchronized with double thymidine blockade (12 hours with 2 mM thymidine, 12 hours release, and 12 hours with 2 mM thymidine), and cells were taken after 2 hours release (S phase) and 8 hours release (G2/M phase). Keywords: time course Comparison of mRNAs measured at S phase (2 hours release after double thymidine blockade) and at G2/M phase (8 hours release after double thymidine blockade); 3 biological replicates at each of the two time points; two technical replicates with dye swapping per comparison; additional comparison between G2/M (8h) and S (2h).

2010-05-07 | E-GEOD-15547 | biostudies-arrayexpress

H3K9K14ac ChIP-chip in lung cancer cells treated with histone deacetylase inhibitor

Project description:Lung cancer is the leading cause of cancer mortality worldwide, yet the therapeutic strategy for advanced non-small cell lung cancer (NSCLC) is limitedly effective. In addition, validated histone deacetylase (HDAC) inhibitors for the treatment of solid tumors remain to be developed. Here, we propose a novel HDAC inhibitor, OSU-HDAC-44, as a chemotherapeutic drug for NSCLC. OSU-HDAC-44 was a pan-HDAC inhibitor and exhibits 3-4 times more effectiveness than suberoylanilide hydroxamic acid (SAHA) in suppressing cell viability in various NSCLC cell lines. Upon OSU-HDAC-44 treatment, mitosis and cytokinesis were inhibited and subsequently led to mitochondria-mediated apoptosis. The cytokinesis inhibition resulted from OSU-HDAC-44-mediated degradation of mitosis and cytokinesis regulators Auroroa B and survivin. The deregulation of F-actin dynamics induced by OSU-HDAC-44 was associated with reduction in RhoA activity resulting from srGAP1 induction. Chromatin-immunoprecipitation-on-chip analysis revealed that OSU-HDAC-44 induced chromatin loosening and facilitated transcription of genes involved in crucial signaling pathways such as apoptosis, axon guidance and protein ubiquitination. Finally, OSU-HDAC-44 efficiently inhibited A549 xenograft tumor growth and induced acetylation of histone and non-histone proteins and apoptosis in vivo. Collectively, our data provide compelling evidence that OSU-HDAC-44 is a potent HDAC targeted inhibitor and can be tested for NSCLC chemotherapy. ChIP-chip analysis for H3K9K14ac in A549, H1299 and CL1-1 lung cancer cells treated with 2.5 uM histone deacetylase inhibitor, OSU-HDAC-44, for 2 hours.

2010-12-22 | E-GEOD-20304 | biostudies-arrayexpress

ChIP-seq analysis with an antibody directed against the human Rad21 protein in Raji cells (Genbank: KF717093.1) prior to and post induction of BZLF1.

Project description:Peaks were identified in both the human and viral (EBV (Human Herpesvirus 4; GenBank accession KF717093.1) genome.

2021-06-22 | E-MTAB-8424 | biostudies-arrayexpress