Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

57 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

U937 scramble vs shHDAC2 upon SAHA (Vorinostat; suberoylanilide hydroxamic acid) treatment

ABSTRACT: Transcriptional profiling of U937 scramble vs shHDAC2 before and after SAHA treatment at 5ÂµM concentration for 6 and 24 hours. Different Experimental Conditions: U937 scramble (U937 trasfected with empty vector) vs shHDAC2 (U937 trasfected with shHDAC2 vector), untreated and treated with SAHA at 5 ÂµM concentration for 6h and 24h. Biological replicates: 2 for each sample, independently grown and harvested at 6 and 24 hours. One replicate per array.

ORGANISM(S): Homo sapiens

SUBMITTER: Mariarosaria Conte

PROVIDER: E-GEOD-37529 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

HDAC2 deregulation in tumorigenesis is causally connected to repression of immune modulation and defense escape.

Conte Mariarosaria M Dell'Aversana Carmela C Benedetti Rosaria R Petraglia Francesca F Carissimo Annamaria A Petrizzi Valeria Belsito VB D'Arco Alfonso Maria AM Abbondanza Ciro C Nebbioso Angela A Altucci Lucia L

Oncotarget 20150101 2

Histone deacetylase 2 (HDAC2) is overexpressed or mutated in several disorders such as hematological cancers, and plays a critical role in transcriptional regulation, cell cycle progression and developmental processes. Here, we performed comparative transcriptome analyses in acute myeloid leukemia to investigate the biological implications of HDAC2 silencing versus its enzymatic inhibition using epigenetic-based drug(s). By gene expression analysis of HDAC2-silenced vs wild-type cells, we found ...[more]

PMID: 25473896

Similar Datasets

An integrated systems biology approach reveals positive and negative effects of suberoylanilide hydroxamic acid (SAHA) on HIV reactivation from latency

Project description:Suberoylanilide hydroxamic acid (SAHA) has been assessed in clinical trials as part of a “shock and kill” strategy to cure HIV-infected patients. While it was effective at inducing expression of HIV RNA "shock" , treatment with SAHA did not result in the reduction of reservoir size "kill". We therefore utilized a systems biology approach to dissect the mechanisms of action of SAHA that may explain its limited success in “shock and kill” strategies. CD4+ T cells from HIV seronegative donors were treated with 1 uM SAHA or its solvent dimethyl sulfoxide for 24 hours. Differential protein expression and post-translational modification was measured with two-dimensional liquid chromatography - tandem mass spectrometry iTRAQ proteomics. Gene expression changes were assessed by Illumina microarrays. Using limma package in the R computing environment, we identified 185 proteins, 18 phosphorylated forms, 4 acetylated forms and 2,982 genes, whose expression was modulated by SAHA. A protein interaction network integrating these 4 data types identified the transcriptional regulator HMGA1 to be upregulated by SAHA at the transcript, protein and acetylated protein levels. HMGA1 has been shown to repress HIV transcription, which is not optimal with respect to a shock and kill strategy. Further functional category assessment of proteins and genes modulated by SAHA identified gene ontology terms related to NFB signaling, protein folding and autophagy, which are all relevant to HIV reactivation. In summary, this study identified a number of host factors that may be therapeutically targeted to achieve more potent HIV reactivation in the “shock and kill” treatment, when using SAHA, either through modification of SAHA itself or through combination with other latency reversing agents. Finally, proteome profiling highlighted a number of potential adverse effects of SAHA, which transcriptome profiling alone would not have identified.

2015-09-10 | PXD002150 | Pride

Global mRNA expression profiling of murine primary PDAC cells following JQ1 or SAHA monotherapy as well as JQ1-SAHA combination therapy

Project description:Global mRNA expression profiles of murine primary PDAC cells following JQ1 or SAHA monotherapy as well as JQ1-SAHA combination therapy were collected using Affymetix mouse whole genome array (Mouse Genome 430A 2.0 Array) . Primary PDAC cells isolated from Ptf1aCre/+;Kras+/LSL-G12D;p53lox/lox (Kras;p53) mice were treated either with JQ1 (100 nM) or SAHA (2000 nM) or vehicle 10% (2-Hydroxypropyl)-β-cyclodextrin (Sigma-Aldrich) or as combination therapy with the indicated dosage for monotherapy. Total RNA isolation was performed after 6 hours of treatment. Primary PDAC cells from Ptf1aCre/+;Kras+/LSL-G12D;p53lox/lox (Kras;p53) mice treated either with JQ1, SAHA, vehicle or JQ1-SAHA combination were analyzed by global gene expression analysis.

2015-09-20 | E-GEOD-64836 | biostudies-arrayexpress

Distinct DNA-based epigenetic switches trigger transcriptional activation of silent genes in human dermal fibroblasts (Affymetrix)

Project description:Artificial epigenetic switches are of increasing demand owing to the critical role of the dynamic epigenome in orchestrating genome-wide transcriptional activation. Recently, we divulged that certain epigenetically active small molecules called SAHA-PIPs containing the cell permeable pyrrole-imidazole polyamides (PIPs) as DNA recognition module and a histone deacetylases inhibitor SAHA as functional module, is capable of triggering targeted transcriptional activation of pluripotency and germ cell genes in mouse and human fibroblasts, respectively. Through microarray studies and functional analysis, here we demonstrate the first ever example about the remarkable ability of 32 different SAHA-PIPs to trigger transcriptional activation of their own unique set of genes and noncoding RNAs. QRT-PCR studies validated that certain SAHA-PIPs could induce several therapeutically important genes including KSR2 and SEMA6A to suggest its potential use as reagents capable of targeted transcriptional activation and as probe(s) to identify the functional relevance of the uncharacterized genes. Gene induction by a SAHA-PIP and SAHA was measured after treating human dermal fibroblasts at 48 h time-point. Experiment includes a vehicle (DMSO) treatment as a negative control.

2013-12-31 | E-GEOD-53316 | biostudies-arrayexpress

U937 ctrl vs U937 Saha (Vorinostat; suberoylanilide hydroxamic acid) 6h

Project description:miRNA expression profiling of U937 ctrl vs U937 treated Saha 5 µM 6h

2017-05-22 | GSE69957 | GEO

Distinct DNA-based epigenetic switches trigger transcriptional activation of silent genes in human dermal fibroblasts (Agilent 2-color)

2013-12-31 | E-GEOD-53318 | biostudies-arrayexpress

Distinct DNA-based epigenetic switches trigger transcriptional activation of silent genes in human dermal fibroblasts (Agilent 1-color)

Project description:Artificial epigenetic switches are of increasing demand owing to the critical role of the dynamic epigenome in orchestrating genome-wide transcriptional activation. Recently, we divulged that certain epigenetically active small molecules called SAHA-PIPs containing the cell permeable pyrrole-imidazole polyamides (PIPs) as DNA recognition module and a histone deacetylases inhibitor SAHA as functional module, is capable of triggering targeted transcriptional activation of pluripotency and germ cell genes in mouse and human fibroblasts, respectively. Through microarray studies and functional analysis, here we demonstrate the first ever example about the remarkable ability of 32 different SAHA-PIPs to trigger transcriptional activation of their own unique set of genes and noncoding RNAs. QRT-PCR studies validated that certain SAHA-PIPs could induce several therapeutically important genes including KSR2 and SEMA6A to suggest its potential use as reagents capable of targeted transcriptional activation and as probe(s) to identify the functional relevance of the uncharacterized genes. Gene induction by each individual SAHA-PIP was measured after treating human dermal fibroblasts at 48 h time-point. Two libraries of SAHA-PIPs (SAHA-PIP 1-16 and 17-32) were investigated in different experiments and each experiment includes a vehicle (DMSO) treatment as a negative control.

2013-12-31 | E-GEOD-53317 | biostudies-arrayexpress

Microarray Analysis of Genes Regulated by Macrophage-Conditioned Media Treatment of Human Adipocytes

Project description:A major development in obesity research is the recognition that the condition is characterized by chronic mild inflammation. Within adipose tissue, this involves the infiltration of macrophages as well as a direct inflammatory response of adipocytes. This study has used Agilent whole-genome microarrays to examine the effects of macrophage-conditioned medium on the global inflammatory response of human adipocytes. Human adipocytes (SGBS cells), differentiated in culture, were treated with macrophage (U937 cells) conditioned media for 4 or 24 h. Control SGBS cells were treated with unconditioned media (control) or RPMI media alone to control for differences in media used to culture U937 cells. There were 6 replicates per group.

2010-04-08 | E-GEOD-14312 | biostudies-arrayexpress

Genome-wide analysis of parental wild-type and derived doxorubicin resistant SK-N-SH neuroblastoma cell lines as well as those co-treated with the histone deacetylase inhibitor SAHA

Project description:Analysis of varied biologic pathways in neuroblastoma SK-N-SH cells grown in doxorubicin and/or SAHA. The hypothesis was that SK-N-SH cells undergo a mesenchymal change through mesenchymal change resulting in a more invasive as well as drug resistant phenotype, and that the mechanism of SAHAs effect on drug resistance may be revealed through this analysis. Total RNA was isolated from wild type, SAHA treated wild type cells, doxorubicin resistant, and SAHA treated doxorubicin resistant SK-N-SH cell lines in triplicate.

2016-05-31 | E-GEOD-47668 | biostudies-arrayexpress

Genome-wide analysis of parental and wild-type SK-N-Be(2)C neuroblastoma cell lines as well as those co-treated with the histone deacetylase inhibitor SAHA

Project description:Analysis of varied biologic pathways in neuroblastoma SK-N-Be(2)C cells grown in doxorubicin and/or SAHA. We hypothesized that SK-N-Be(2)C cells undergo a mesenchymal change through mesenchymal change resulting in a more invasive as well as drug resistant phenotype, and that the mechanism of SAHAs effect on drug resistance may be revealed through this analysis. Total RNA was isolated from wild type, SAHA treated wild type cells, doxorubicin resistant, and SAHA treated doxorubicin resistant SK-N-Be(2)C cell lines in triplicate.

2016-05-31 | E-GEOD-47669 | biostudies-arrayexpress

Global mRNA expression profiling of patient derived pancreatic carcinoma xenograft Bo63 following JQ1-SAHA combination therapy

Project description:Global mRNA expression profiling of patient derived pancreatic carcinoma xenograft Bo63 were collected using Agilent human whole genome array (G4845A AMADID 026652, cRNA 4x44k V2) . Two different sources of RNA were analyzed: 1.) Bo63 xenograft tumors grown on nude mice treated with vehicle only as control. 2.) Bo63 xenograft tumor grown on nude mice treated with JQ1 and SAHA (SAHA 25 mg/kg 1-0-0 and JQ1 50 mg/kg 0-0-1, treatment was imitated when tumor size reached 200 mm³ +/- 20 mm³. Two conditions (vehicle vs JQ1-SAHA treatment), each condition is represented by 3-4 biological replicates

2015-09-20 | E-GEOD-64837 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data