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Identification of differentially expressed genes due to LBH589 treatment in aromatase inhibitor-resistant tumors

ABSTRACT: In order to validate the utility of a novel pathway algorithm (BD-Func), we test if an LBH589 signature based data from 3 cell lines (GSE36509) in an independent experiment in vivo.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47346 | GEO | 2014/03/10

SECONDARY ACCESSION(S): PRJNA205203

REPOSITORIES: GEO

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Identification of differentially expressed genes due to LBH589 treatment in aromatase inhibitor-resistant tumors

Project description:In order to validate the utility of a novel pathway algorithm (BD-Func), we test if an LBH589 signature based data from 3 cell lines (GSE36509) in an independent experiment in vivo. Xenograft tumor treatment (see Kubo et al. 2012; PMID 23160924), microarray gene expression profiling, functional analysis using BD-Func. Mouse xenograft (from MCF-7aro cell line) was treated with exemestane (EXE) or EXE + LBH589.

2014-03-10 | E-GEOD-47346 | biostudies-arrayexpress

Identification of differentially expressed genes in LBH589-treated cells

Project description:To identify the targets of LBH589 treatment, we compared gene expression profiles in three different types of human cancer cell lines (H295R, HeLa and MCF-7her2) with and without LBH589 treatment. Affymetrix microarray analysis was performed to determine changes in gene expression that are unique to LBH treatment.

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Identification of differentially expressed genes in LBH589-treated cells

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SK-NEP-1 treated with LBH589

Project description:Wilms tumor (WT) is an embryonic kidney cancer, for which histone acetylation might be a therapeutic target. LBH589, a novel targeted agent, suppresses histone deacetylases in many tumors. This study investigated the antitumor activity of LBH589 in SK-NEP-1 cells. LBH589 inhibited cell proliferation of SK-NEP-1 cells in a dose-dependent manner. Annexin V, Tunel and Hochest 33342 staining analysis showed that LBH589-treated cells showed more apoptotic features compared with the control. LBH589 treatment inhibited the growth of SK-NEP-1 xenograft tumors in nude mice. Arraystar Human LncRNA Array analysis of genes and lncRNas regulated by LBH589 identified 6653 mRNAs and 8135 lncRNAs in LBH589-treated SK-NEP-1 cells. The most enriched gene ontology terms were those involved in nucleosome assembly. KEGG pathway analysis identified cell cycle proteins, including CCNA2, CCNB2, CCND1, CCND2, CDK4, CDKN1B and HDAC2, etc. Ingenuity Pathway Analysis identified important upstream molecules: HIST2H3C, HIST1H4A, HIST1A, HIST1C, HIST1D, Histone H1, Histone H3, RPRM, HSP70 and MYC.

2015-12-30 | GSE64975 | GEO

LBH589 (Panobinostat) treatment of a gastric cancer cell line

Project description:LBH589 is a histone deacetylase (HDAC) inhibitor, treatment and changes in acetylated histones alters gene expression Gastric cancer cell line AGS was treated with 100nM LBH589 for 24h.

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LBH589 (Panobinostat) treatment of a gastric cancer cell line

Project description:LBH589 is a histone deacetylase (HDAC) inhibitor, treatment and changes in acetylated histones alters gene expression

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Transcriptome analysis after treating with LBH589 in ocular melanoma cells

Project description:In order to study the mechanism of histone acetylation affecting development of ocular melanoma, we treated ocular melanoma cells with histone deacetylatase inhibitor LBH589. The results showed that the METTL14 was increased after LBH589 treatment. The study aims to reveal the interaction between histone acetylation and m6A modification, and to further explore the relationship between the expression level of METTL14 and the survival time of ocular melanoma patients, hopefully providing new ideas for the treatment of malignant tumors.

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Microarray expression data following the treatment of mouse ESC with Panobinostat/LBH589

Project description:Histone acetylation is a dynamic modification regulated by the opposing actions of histone acetyltransferases and histone deacetylases (HDACs). Deacetylation of histone tails results in chromatin tightening and therefore HDACs are generally regarded as transcriptional repressors. Counterintuitively, simultaneous deletion of HDAC1 and HDAC2 in embryonic stem cells (ESC) reduced expression of pluripotent transcription factors, Oct4, Sox2 and Nanog (OSN). By shaping global histone acetylation HDACs indirectly regulate the activity of acetyl-lysine readers, such as BRD4. To examine the direct effects of HDAC (LBH589) and BRD4 (JQ1) inhibition on the ESC transcriptome, we performed precision nuclear run-on and sequencing (PRO-seq) analysis. Both LBH589 and JQ1 caused a marked reduction in the pluripotent network. However, while JQ1 treatment induced widespread transcriptional pausing of genes, HDAC inhibition caused a reduction in both paused and elongating polymerase, suggesting an overall reduction in recruitment of RNAPII. Using enhancer RNA (eRNA) expression to measure enhancer activity, we found that while HDAC activity regulates fewer enhancers than JQ1, LBH589 sensitive eRNAs were preferentially associated with super-enhancers and OSN binding sites. These findings suggest that HDAC activity is required for maintenance of pluripotency by regulating the OSN enhancer network via optimal recruitment of RNA polymerase II. Comparative gene expression using the Illumina mouseWG-6 v2 expression BeadChip platform. The effects of Panobinostat/LBH589 (50nM)

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Phase II Trial of LBH589 in Refractory Colorectal Cancer

Project description:The purpose of this study is to determine the effects of the study drug, LBH589, on patients with metastatic colorectal cancer that has continued to grow despite previous treatment.

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The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (SNP)

Project description:Histone deacetylases (HDACs) have been identified as therapeutic targets due to regulatory function in DNA structure and organization. We have analyzed the role of the LBH589, a novel pan inhibitor of class I and II HDACs, in Acute Lymphoblastic Leukemia. In vitro, LBH589 was shown to induce a dose dependent antiproliferative and apoptotic effect which was associated with an increase in the acetylation of H3 and H4 histone acetylation which was uniformly in every genetic subgroup of ALL. In vivo administration of LBH589 in BALB/c-RAG2-/-γc-/- mice in which T and B-cell leukemic cell lines were injected induced a significant reduction in tumor growth (TOM-1, p<0.01 and MOLT-4 p<0.05). Leukemic cells from patients were employed to establish a xenograft model of human leukemia in BALB/c-RAG2-/-γc-/- mice and further transplanted in consecutive generations of mice. Treatment of these xenografts with LBH589 induced an increase in the acetylation of H3 and H4 and prolonged the survival of mice in comparison with the animals treated with Vincristine and Dexametasone (p<0.05) and this effect was significantly higher when LBH589 was combined with Vincristine and Dexametasone (p<0.001). Our results that the use of LBH589 in combination with standard chemotherapy represents an attractive option for treatment of patients with ALL.

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