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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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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. 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

ORGANISM(S): Homo sapiens

SUBMITTER: John Halsall

PROVIDER: E-GEOD-65297 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2015-08-31 | GSE65297 | GEO

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

U937 miR-194-5p (UmiR-194-5p) vs U937 miR-194-5p (UmiR-194-5p) treated with SAHA (Vorinostat; suberoylanilide hydroxamic acid)

Project description:Transcriptional profiling of U937 miR-194-5p (UmiR-194-5p) vs U937 miR-194-5p (UmiR-194-5p) treated with SAHA (Vorinostat; suberoylanilide hydroxamic acid) for 24 h at 5uM concetration

2017-05-22 | GSE73648 | GEO

Transcription profiling by array of human gastric cancer cells treated with suberoylanilide hydroxamic acid (SAHA)

Project description:Gastric cancer cell line AGS was treated with suberoylanilide hydroxamic acid (SAHA) for 24 hours. Microarray analysis was done to explore the differentially expressed genes betweenSAHA treated and control cells.

2011-05-01 | E-MEXP-2695 | 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

Suberoylanilide Hydroxamic Acid, Fluorouracil, Leucovorin, and Oxaliplatin in Treating Patients With Progressive Metastatic or Unresectable Colorectal Cancer or Other Solid Tumors

Project description:This phase I trial is studying the side effects and best dose of suberoylanilide hydroxamic acid when given together with fluorouracil, leucovorin, and oxaliplatin in treating patients with progressive metastatic or unresectable colorectal cancer or solid tumor. Drugs used in chemotherapy, such as suberoylanilide hydroxamic acid, fluorouracil, leucovorin, and oxaliplatin, work in different ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing. Suberoylanilide hydroxamic acid may also stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Giving more than one drug (combination chemotherapy) may kill more tumor cells.

| 2014859 | ecrin-mdr-crc

A Clinical Trial of Oral Suberoylanilide Hydroxamic Acid (SAHA) in Patients With Relapsed or Refractory Breast, Colorectal and Non-Small Cell Lung Cancer (0683-011)(TERMINATED)

Project description:This is an investigational study to determine the response rate of relapsed/refractory breast, colorectal and non-small cell lung cancer to oral suberoylanilide hydroxamic acid (SAHA), to evaluate PET as an earlier indicator of response to SAHA as assessed by response evaluation criteria in solid tumours (RECIST) criteria and to evaluate the safety and tolerability of oral suberoylanilide hydroxamic acid.

| 2013972 | ecrin-mdr-crc

SAHA, VPA and JQ1 treatment in ISOS-1

Project description:ISOS-1, a mouse angiosarcoma cell line, was treated with histone deacetyltransferase inhibitors (HDACI: SAHA and VPA) and a bromodomain and extraterminal domain inhibitor (BETi: JQ1).

2022-05-10 | GSE200106 | GEO

A Window of Opportunity Study of Valproic Acid in Breast Cancer Testing a Gene Expression Biomarker

Project description:Purpose: Valproic acid(VPA) has anti-cancer activity attributed to histone deacetylase inhibition(HDACi). We published the Genomically–Derived Sensitivity Signature for VPA(GDSS-VPA), a gene expression biomarker predicting breast cancer sensitivity to VPA in vitro and in vivo. We conducted a window-of-opportunity study examining the tolerability of VPA and the ability of the GDSS-VPA to predict biologic changes in breast tumors from VPA. Methods: Eligible women had untreated breast cancer with breast tumors over 1.5 cm. After a biopsy, women took VPA for 7-12 days, increasing from 30mg/kg/day PO divided BID to a maximum of 50mg/kg/day. After VPA treatment, serum VPA level was measured followed by breast surgery or a biopsy. Tumor proliferation was assessed by Ki-67 immunohistochemistry. Peripheral blood mononuclear cells(PBMCs) histone acetylation was assessed by Western blot. Results: Thirty women were evaluable. The median age was 54(range 31-73). 52% of women tolerated 50mg/kg/day, but 10% missed more than two doses due to adverse events(AEs). Grade 3 AEs included one patient with vomiting and diarrhea and one with fatigue. The end serum VPA level correlated with change in PBMC histone acetylation(rho=0.451, p=0.024). 50% of women with triple-negative breast cancer(TNBC) had a Ki-67 reduction of at least 10%, compared with 17% of other women. GDSS-VPA correlated with a Ki-67 decrease of at least 10%(AUC 0.66). Conclusions: Most women tolerate VPA. VPA treatment caused a decrease in proliferation of breast tumors. The genomic biomarker correlated with decreased proliferation. HDACi is a valid strategy for drug development in TNBC using gene expression biomarkers.

2016-12-17 | GSE83530 | GEO

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