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Transcriptional response to histone deacetylase inhibitors

ABSTRACT: Histone deacetylase inhibitors are a class of drug which rapidly induce hyperacetylation of histone proteins. Here, we aimed to study the association between HDACi-induced histone acetylation and changes in gene expression. To study the early responses to HDACi treatment we treated cells with three different concentrations of two HDACi, sodium valproate (VPA) and suberoylanilide hydroxamic acid over a short timecourse.

ORGANISM(S): Homo sapiens

PROVIDER: GSE65297 | GEO | 2015/08/31

SECONDARY ACCESSION(S): PRJNA273641

REPOSITORIES: GEO

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Transcriptional response to histone deacetylase inhibitors

Project description:Histone deacetylase inhibitors are a class of drug which rapidly induce hyperacetylation of histone proteins. Here, we aimed to study the association between HDACi-induced histone acetylation and changes in gene expression. To study the early responses to HDACi treatment we treated cells with three different concentrations of two HDACi, sodium valproate (VPA) and suberoylanilide hydroxamic acid over a short timecourse. AH LCL cells were treated with 0.2mM, 1mM or 5mM valproic acid (VPA) or 0.5, 2.5 or 12.5µM suberoylanilide hydroxamic acid (SAHA). GM12878 cells were treated with 1mM VPA. Samples were collected at 0, 30, 60 and 120 minutes. All experiments were carried out in triplicate. One replicate of AH LCL, 0.2mM VPA, 30min and one replicate of AH LCL, 5mM VPA, 30min were eliminated as outliers

2015-08-31 | E-GEOD-65297 | biostudies-arrayexpress

Expression data from human hepatic stellate cell line LX2 treated with suberoylanilide hydroxamic acid (SAHA) or valproic acid (VPA)

Project description:Suberoylanilide hydroxamic acid (SAHA) and valproic acid (VPA) are both histone deacetylases inhibitor (HDACi), and are able to attenuate the activation of hepatic stelllate cells. To explore the underlying molecular mechanisms, we performed gene expression profile analyses of human hepatic stellate cell line LX2 treated with SAHA or VPA for 24 hours. Duplicate experiments were performed: Untreated LX2, SAHA treated LX2 and VPA treated LX2.

2016-04-07 | E-MTAB-3764 | biostudies-arrayexpress

miRNA expression data from human hepatic stellate cell line LX2 treated with suberoylanilide hydroxamic acid (SAHA) or valproic acid (VPA)

Project description:Suberoylanilide hydroxamic acid (SAHA) and valproic acid (VPA ) are both histone deacetylases inhibitor (HDACi), and are able to attenuate the activation of hepatic stelllate cells. To explore the underlying molecular mechanisms, we performed miRNA expression profile analyses of human hepatic stellate cell line LX2 treated with SAHA or VPA for 24 hours. Duplicate experiments were performed: Untreated LX2, SAHA treated LX2 and VPA treated LX2.

2019-07-20 | E-MTAB-6752 | biostudies-arrayexpress

Histone deacetylase inhibition mitigates fibrosis-driven disease progression in recessive dystrophic epidermolysis bullosa

Project description:To delineate sodium valproate (VPA) molecular effects underlying mitigation of skin fibrosis in RDEB mice, mass spectrometry-based expression proteomics was performed on protein extracts from back skin of 16 weeks-old VPA-treated RDEB mice, vehicle-treated RDEB mice and WT littermates.

2024-08-31 | PXD047998 | Pride

Epigenetic evidence of an Ac/Dc axis by VPA and SAHA

Project description:Valproic acid (VPA) is one of the most commonly used anti-epileptic drugs with pharmacological actions on GABA and blocking voltage-gated ion channels. VPA also inhibits histone deacetylase (HDAC) activity. Suberoylanilide hydroxamic acid is also a member of a larger class of compounds that inhibit HDACs. At the time of this article, there are 123 active international clinical trials for VPA (also known as valproate, convulex, divalproex, and depakote) and SAHA (vorinostat, zolinza). While it is well known that VPA and SAHA influence the accumulation of acetylated lysine residues on histones, their true epigenetic complexity remains poorly understood. Primary human cells were exposed to VPA and SAHA to understand the extent of histone acetylation (H3K9/14ac) using chromatin immunoprecipitation followed by sequencing (ChIP-seq). Because histone acetylation is often associated with modification of lysine methylation, we also examined H3K4me3 and H3K9me3. To assess the influence of the HDAC inhibitors on gene expression, we used RNA sequencing (RNA-seq).

2024-09-04 | GSE276338 | GEO

Combining Sodium Valproate With Standard-of-care EGFR (Epidermal Growth Factor Receptor) Monoclonal Antibody Treatment in Patients With Metastatic Colorectal Cancer

Project description:The aim of this study is to determine the efficacy of combining the histone deacetylase (HDAC) inhibitor sodium valproate (VPA) with anti-EGFR monoclonal antibody (panitumumab or cetuximab) maintenance in the first-line treatment of patients with RAS wild type metastatic CRC.

| 5791 | ecrin-mdr-crc

Gene expression profile of mouse ES cells treated with 1mM valproic acid for 8 hours

Project description:Histone deacetylase inhibitors (HDACi) cause hyperacetylation of bulk histones and H3K4 hypermethylation in a variety of cell types. They find clinical application as anti-epileptics and chemotherapeutic agents, but the pathways through which they alter cell physiology remain unclear. Surprisingly, changes in gene expression caused by HDACi are often limited in extent and can be positive or negative. Here we have explored the ability of the clinically important HDACi valproic acid (VPA) to alter gene expression in mouse embryonic stem (ES) cells.

2013-03-29 | GSE45610 | GEO

Profile of gene expression in K562 cells exposed to 2 mM sodium valproate for 12 hours using Agilent SurePrint G3 Human GE 8x60K Microarray.

Project description:To explore the mechanism underlying anti-leukaemia effect of sodium valproate, the growth and survival of the K562 cell line were investigated using the Annexin V/PI dual staining method. Global profiles of gene expression in K562 cells exposed to sodium valproate were assessed using gene expression microarray and validated by qRT-PCR. Gene ontology analysis was performed to establish the function of differentially expressed genes. The differentially expressed genes identified by using gene expression array were further used to query the CMAP database to retrieve a ranked list of compounds that act on the same intracellular targets as sodium valproate. A significant increase in cell apoptosis was observed in valproate exposed K562 cells using flow cytometry. A total of 706 transcripts were identified as being significantly differentially expressed. Eight differentially expressed genes that might be involved in apoptosis were verified by qRT-PCR. The significant enrichment analysis of gene ontology terms for the differentially expressed genes revealed that these genes are involved in many important biological processes such as apoptosis. The connectivity map analysis showed gene expression profile in K562 cells exposed to sodium valproate observed in this study was most similar to that of HDACi and PI3K inhibitor in the connectivity map database, suggesting that sodium valproate might exert anti-leukaemic action by inhibiting HDAC as well as inhibiting PI3K pathway. In conclusion, the data obtained in this study might provide the ground for further studies to elucidate the molecular and therapeutic potential of VPA in leukaemia treatment.

2011-11-11 | GSE32189 | GEO

Profile of gene expression in K562 cells exposed to 2 mM sodium valproate for 12 hours using Agilent SurePrint G3 Human GE 8x60K Microarray.

2011-11-11 | E-GEOD-32189 | biostudies-arrayexpress

Acquired resistance of Jurkat cells to TNF-related apoptosis-inducing ligand (TRAIL): a role for histone deacetylase inhibitors as powerful apoptosis sensitizer.

Project description:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to be a potent inducer of apoptosis in various cancer cell lines and primary cancer cells. However, in clinical trials administration of recombinant TRAIL or TRAIL death receptor agonists did not show sufficient efficacy for treatment of tested malignant disorders compared to standard chemotherapy. Acquired resistance of cancer cells to TRAIL and to other âdeath receptorâ ligands may explain not only the inability of TRAIL and TRAIL âdeath receptorâ agonists to achieve the clearance of cancer cells in vivo but also the escape of cancer cells from immune cell â mediated killing. Selective pressure of TRAIL on TRAIL-sensitive Jurkat T-lymphoblastic leukemia cells provided several TRAIL resistant Jurkat cell line clones (TR1, TR2, TR3). Irrespective of molecular changes histone deacetylase inhibitors (HDACi), such as suberoylanilide-hydroxamic acid (SAHA, vorinostat), were able to restore sensitivity of all three TRAIL-resistant clones to TRAIL. Gene expression analysis of TR1 clone treated with SAHA 1microM for 12 hours compared to untreated TR1 clone showed significant decrease in expression of CFLAR/cFLIP (0.71; p=0.006), BIRC5/survivin (0.80; p=0.024) and BID (0.66; p<0.001). Expression of both TRAIL âdeathâ receptors DR4 (1.57; p<0.001) and DR5 (1.47; p=0.002) were significantly increased compared to untreated TR1 cells. The mRNA expression of caspases-2,-3,-8,-9,-10 did not significantly change with the SAHA treatment. Total cellular RNA was isolated from biologic duplicates of untreated Jurkat cells (WT), TRAIL resistant Jurkat cell clone (TR1) and 1 ÂµM and 0.5 ÂµM suberoylanilide-hydroxamic acid (SAHA, vorinostat) treated TR1 cell clones for 12 hours. Jurkat cell line subclones TR1was established by selective pressure of TRAIL 1000 ng/mL on Jurkat cells over the period of 12 weeks.

2016-06-15 | E-GEOD-38745 | biostudies-arrayexpress

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