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SAHA CCMS - SAHA Capture Compound--a novel tool for the profiling of histone deacetylases and the identification of additional vorinostat binders

ABSTRACT: SAHA CCMS in HepG2

INSTRUMENT(S): LTQ-Orbitrap

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Hepatocyte

SUBMITTER: Jenny J. Fischer

LAB HEAD: Jenny J. Fischer

PROVIDER: PRD000443 | Pride | 2011-10-19

REPOSITORIES: Pride

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			Action	DRS
	PRIDE_Exp_Complete_Ac_17666.pride.mgf.gz	Mgf
	PRIDE_Exp_Complete_Ac_17666.pride.mztab.gz	Mztab
	PRIDE_Exp_Complete_Ac_17666.xml.gz	Xml
	PRIDE_Exp_Complete_Ac_17667.pride.mgf.gz	Mgf
	PRIDE_Exp_Complete_Ac_17667.pride.mztab.gz	Mztab

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Publications

SAHA Capture Compound--a novel tool for the profiling of histone deacetylases and the identification of additional vorinostat binders.

Fischer Jenny J JJ Michaelis Simon S Schrey Anna K AK Diehl Anne A Graebner Olivia Y OY Ungewiss Jan J Horzowski Sabine S Glinski Mirko M Kroll Friedrich F Dreger Mathias M Koester Hubert H

Proteomics 20110907 20

Suberoylanilide hydroxamic acid (SAHA) is a potent histone deacetylase (HDAC) inhibitor. Inhibitors of HDACs are used in cancer therapy based on the role HDACs play in transcription by regulating chromatin compaction and non-histone proteins such as transcription factors. Profiling of HDAC expression is of interest in the functional proteomics analysis of cancer. Also, non-HDAC proteins may interact with HDAC inhibitor drugs and contribute to the drug mode of action. We here present a tool for t ...[more]

PMID: 21898820

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Histone deacetylases inhibition by SAHA/Vorinostat normalizes the glioma microenvironment via xCT equilibration.

Project description: Not available

| S-EPMC4165982 | biostudies-literature

Differential Transcriptomic Modulation by Histone Deacetylase Inhibitor SAHA in LUAD and LUSC

Project description:Background: Histone deacetylases (HDACs) drive non-small-cell lung cancer (NSCLC) progression, yet HDAC inhibitor (HDACi) responses vary by tumor subtype. We compared the pan-HDAC inhibitor SAHA (vorinostat) in two NSCLC models-HER2-mutant lung adenocarcinoma (NCI-H1299; TP53del, NRASQ61K) and EGFR/PI3K-driven squamous carcinoma (NCI-H1703; PDGFRAamp, PIK3CAE542K)-to uncover lineage-specific mechanisms. Methods: Cells were treated with SAHA (10 µM, 24 h), a clinically relevant dose yielding ~1 µM free drug in plasma. Strand-specific RNA-seq was aligned to GRCh38.p13 and analyzed with edgeR and DESeq2 (FDR < 0.05, |Log₂FC|≥ 1). Pathway, protein-interaction, apoptosis (Annexin V/PI), and migration (scratch, trans-well + mitomycin C) assays complemented transcriptomics. Clinical relevance was assessed by correlating SAHA-regulated genes with disease-free survival in TCGA-LUAD and TCGA-LUSC via GEPIA2. Results: SAHA altered 1098 genes in H1299 and 1532 in H1703, with only 437 shared. In H1299, SAHA induced EMT and MAPK-feedback genes while repressing interferon/apoptosis pathways. In H1703, SAHA activated complement/ECM remodeling and suppressed cell-cycle regulators. Class II HDACs (HDAC4/6) were downregulated only in H1703. Functionally, H1703 exhibited greater apoptosis; H1299 showed stronger migration inhibition. SAHA-reversed gene signatures (e.g., HMMR, PLK1 in LUAD; PAPPA, SAMD11 in LUSC) were significantly associated with poor disease-free survival, defining HDAC9-HMMR/PLK1 and HDAC4/6-PAPPA/SAMD11 axes. Conclusions: SAHA elicits distinct subtype-specific transcriptional and phenotypic effects in NSCLC. These findings highlight the importance of genetic context in HDACi therapy and support tailored combinations-such as SAHA with MAPK inhibitors in LUAD or HDAC4/6-targeted approaches in LUSC-and the use of SAHA-modulated biomarkers for patient stratification.

2026-02-25 | GSE302469 | GEO

In vivo PET imaging of histone deacetylases by 18F-suberoylanilide hydroxamic acid (18F-SAHA).

Project description: Not available

| S-EPMC3150598 | biostudies-literature

Vascular histone deacetylation by pharmacological HDAC inhibition [SAHA, RNA-seq]

Project description:HDAC inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. Often studied at single loci, increased histone acetylation is the paradigmatic mechanism of action, however, little is known of the extent of genome-wide changes of the mammalian genome when stimulated by the hydroxamic acids, TSA and SAHA. In primary human vascular endothelial cells we map the chromatin modifications, histone H3 acetylation of lysine 9 and 14 (H3K9/14ac) using chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq). Since acetylation mediated gene expression is often associated with modification of other lysine residues we also examined H3K4me3 and H3K9me3 as well as changes in CpG methylation (CpG-seq). Genome-wide mRNA sequencing indicates the differential expression of about 30% of genes, with almost equal numbers being up- and down- regulated. We observe deacetylation conferred by TSA and SAHA that are associated with decreased gene expression. Histone deacetylation is associated with the loss of p300/CBP binding at gene promoters. This study provides an important framework for HDAC inhibitor function in vascular biology and a comprehensive description of genome-wide deacetylation. HAEC mRNA profiles of SAHA treated and control samples were generated by deep sequencing, in triplicate, using Illumina GAIIx.

2014-02-23 | E-GEOD-54912 | biostudies-arrayexpress

Vascular histone deacetylation by pharmacological HDAC inhibition [SAHA, ChIP-seq]

Project description:HDAC inhibitors are thought to regulate gene expression by post-translational modification of histone as well as non-histone proteins. Often studied at single loci, increased histone acetylation is the paradigmatic mechanism of action, however, little is known of the extent of genome-wide changes of the mammalian genome when stimulated by the hydroxamic acids, TSA and SAHA. In primary human vascular endothelial cells we map the chromatin modifications, histone H3 acetylation of lysine 9 and 14 (H3K9/14ac) using chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (ChIP-seq). Since acetylation mediated gene expression is often associated with modification of other lysine residues we also examined H3K4me3 and H3K9me3 as well as changes in CpG methylation (CpG-seq). Genome-wide mRNA sequencing indicates the differential expression of about 30% of genes, with almost equal numbers being up- and down- regulated. We observe deacetylation conferred by TSA and SAHA that are associated with decreased gene expression. Histone deacetylation is associated with the loss of p300/CBP binding at gene promoters. This study provides an important framework for HDAC inhibitor function in vascular biology and a comprehensive description of genome-wide deacetylation. HAEC ChIP-seq profiles for 3 histone marks of SAHA treated and control samples were generated by deep sequencing, in triplicate, using Illumina GAIIx.

2014-02-23 | E-GEOD-54909 | biostudies-arrayexpress

Dissection of anti-tumor activity of histone deacetylase inhibitor SAHA in NPC cells via quantitative phosphoproteomics

Project description:Suberoylanilide hydroxamic acid (SAHA), as a pan HDAC inhibitor, has been approved for clinical use and it has been demonstrated to treat solid tumor. Nevertheless, the mechanism underlying the therapeutic effects of SAHA on tumors are still not fully understood. Protein phosphorylation is one of the most important regulatory events in cells, regulating primary biological processes, such as cell division, growth, migration, differentiation, and intercellular communication. The impact of SAHA treatment on cellular phosphorylation and signaling pathways might contribute to our understanding on its therapeutic mechanism. For this purpose, by combining tandem mass tags(TMT)-based quantitative proteomics and titanium dioxide-based phosphopeptide enrichment, we for the first time comprehensively identified and quantified protein phosphorylation in NPC cells toward SAHA treatment. we identified 7430 phosphorylation sites on 2456 phosphoproteins in the NPC cell line 5-8F, of which 1176 phosphorylation sites on 528 phosphoproteins were significantly expressed upon SAHA treatment. Biological analysis show that SAHA can influence several biological processes including mRNA/DNA processing, cell cycle. Furthermore, signaling pathway analysis demonstrate that SAHA can activate cell cycle regulation related pathway such as p53 signalling pathway, and inactivate energetic pathway such as AMPK pathway etc. Overall, our study presents evidence at a phosphoproteomic level that SAHA can inhibit NPC cell growth by regulating the cell cycle and cell energy metabolism. Our findings will contribute to elucidation of the mechanisms through which SAHA exerts its anticancer effects.

2020-08-20 | PXD021029 |

SAHA Rat Dental Pulp

Project description:Transcriptional response of rat dental pulp cells (DPCs) cultured with SAHA at early and late mineralisation time points Transcript profiling of DPC identified several novel genes expression induced and supressed by HDACi at 24 hrs and 14 days under mineralising conditions. SAHA induces several members of the MMP family of endopepsidases (TIMP-1, MMP-9, MMP-13) and other members of the endochondral ossification pathway at 24 h.

2015-06-16 | GSE67175 | GEO

Effects of SAHA on human gut microbiome

Project description:The human stool samples were collected and processed for in vitro culturing under anaerobic condition using rapidAIM assay with or without SAHA, an lysine deacetylase inhibitor, for evaluating the effects of SAHA on human gut microbiome. Metaproteomics were used to analyze the microbiome composition and functions.

2022-03-01 | PXD016388 | Pride

Effects of suberanilohydroxamic acid (SAHA) on HeLa cells

Project description:Analysis of HeLa cells treated with histone deacetylase inhibitor SAHA for 24hr. Results provide insight into the effect of SAHA on the activation of lysosomal and autophagy pathways

2019-07-08 | GSE106175 | GEO

Expression data in MDA-MB-231 breast cancer cell lines with Histone deacetylase SAHA treatment

Project description:Analysis of gene expression change after 8hr's treatment with 5μM SAHA, which is a histone deacetylase inhibitor, in MDA-MB-231 cell lines.

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