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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Identification of differentially expressed genes in LBH589-treated cells

ABSTRACT: 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. LBH-treated cell lines received 50 nM of LBH589 for 24 hours. DMSO and LBH treatments are in triplicate.

ORGANISM(S): Homo sapiens

SUBMITTER: Shiuan Chen

PROVIDER: E-GEOD-36509 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Inhibition of the proliferation of acquired aromatase inhibitor-resistant breast cancer cells by histone deacetylase inhibitor LBH589 (panobinostat).

Kubo Makoto M Kanaya Noriko N Petrossian Karineh K Ye Jingjing J Warden Charles C Liu Zheng Z Nishimura Reiki R Osako Tomofumi T Okido Masayuki M Shimada Kazuo K Takahashi Masato M Chu Peiguo P Yuan Yate-Ching YC Chen Shiuan S

Breast cancer research and treatment 20121118 1

Aromatase inhibitors (AIs) are important drugs for treating postmenopausal patients with hormone receptor-positive breast cancer. However, acquired resistance to AI therapies is a significant problem. Our study has revealed that the histone deacetylase inhibitor LBH589 treatment abrogated growth of AI-resistant cells in vitro and in vivo, causing cell cycle G2/M arrest and induced apoptosis. LBH589 treatment also reduced the level of NF-κB1 which is overexpressed when AI resistance develops. Ana ...[more]

PMID: 23160924

Similar Datasets

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.

2015-03-02 | GSE36509 | GEO

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

Drosha knock-down gene expression in HSPCs

Project description:Genome-wide expression differences are compared for a normal and mutant cell line. The data compares the effect of a gene mutation on genome-wide expression. empty vector (EV), shDrosha (shDr); shDr denotes hematopoietic stem-progenitor cells (HSPCs) transduced with a short-hairpin RNA targeting the miRNA-processing enzyme Drosha

2016-07-03 | E-GEOD-47403 | biostudies-arrayexpress

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

The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (TOM-1 and MOLT-4)

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-/-gammac-/- 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-/-gammac-/- 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. Three different biological replicates of ALL derive cell lines TOM-1 and MOLT-4 after and before treatment with LBH589

2012-04-17 | E-GEOD-26790 | biostudies-arrayexpress

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

2012-04-15 | GSE36444 | 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.

2012-04-14 | E-GEOD-36444 | biostudies-arrayexpress

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.

2022-10-02 | GSE214457 | GEO

Expression data from MTDH knockdown in the Hec50co endometrial cancer cell line

Project description:Understanding the molecular underpinnings of chemoresistance is vital to design therapies to restore chemosensitivity. In particular, metadherin (MTDH) has been demonstrated to have a critical role in chemoresistance. Over-expression of MTDH has recently been implicated in poor clinical outcome in breast cancer, neroblastoma, hepatocellular carcinoma and prostate cancer. In this present study, we focused on the therapeutic benefit of MTDH depletion to restore sensitivity to cell death mediated by a combinatorial therapy of tumor necrosis factor-alpha-related apoptosis-inducing ligand (TRAIL), which promotes death of cancerous cells of the human reproductive tract, and histone deacetylase (HDAC) inhibitors, which have been shown to increase sensitivity of cancer cells to TRAIL-induced apoptosis. Our data indicate that depletion of MTDH in endometrial cancer cells results in sensitization of cells that were previously resistant to cell death mediated by combinatorial treatment with TRAIL and HDAC inhibitor LBH589. MTDH was found to be involved in G2/M checkpoint regulation in response to LBH589 alone or LBH589 in combination with TRAIL, suggesting that MTDH functions at the cell cycle checkpoint to accomplish resistance.Using microarray technology, we identified 57 downstream target genes of MTDH, including Calbindin 1 and Galectin 1, which may contribute to MTDH-mediated resistance to combinatorial TRAIL and HDAC inhibitor targeted therapy. Inhibition of PDK1,AKT phosphorylation and increase Bim expression and XIAP degradation may result in sensitivity to cell death induction in MTDH depleted Hec50co cells by TRAIL and LBH 589 combination treatment. These findings indicate that depletion of MTDH is a potentially novel avenue for effective cancer therapy. The microarray was performed on three biological triplicates as well as three experimental triplictes of stable knockdown and control cells. MTDH was knocked down using a shRNA.

2010-12-17 | E-GEOD-26134 | biostudies-arrayexpress

Expression data from metadherin (MTDH) knockdown in the Ishikawa H endometrial cancer cell line

Project description:Understanding the molecular underpinnings of chemoresistance is vital to design therapies to restore chemosensitivity. In particular, metadherin (MTDH) has been demonstrated to have a critical role in chemoresistance. Over-expression of MTDH has recently been implicated in poor clinical outcome in breast cancer, neroblastoma, hepatocellular carcinoma and prostate cancer. In this present study, we focused on the therapeutic benefit of MTDH depletion to restore sensitivity to cell death mediated by a combinatorial therapy of tumor necrosis factor-alpha-related apoptosis-inducing ligand (TRAIL), which promotes death of cancerous cells of the human reproductive tract, and histone deacetylase (HDAC) inhibitors, which have been shown to increase sensitivity of cancer cells to TRAIL-induced apoptosis. Our data indicate that depletion of MTDH in endometrial cancer cells results in sensitization of cells that were previously resistant to cell death mediated by combinatorial treatment with TRAIL and HDAC inhibitor LBH589. MTDH was found to be involved in G2/M checkpoint regulation in response to LBH589 alone or LBH589 in combination with TRAIL, suggesting that MTDH functions at the cell cycle checkpoint to accomplish resistance.Using microarray technology, we identified 57 downstream target genes of MTDH, including Calbindin 1 and Galectin 1, which may contribute to MTDH-mediated resistance to combinatorial TRAIL and HDAC inhibitor targeted therapy. Inhibition of PDK1,AKT phosphorylation and increase Bim expression and XIAP degradation may result in sensitivity to cell death induction in MTDH depleted Hec50co cells by TRAIL and LBH 589 combination treatment. These findings indicate that depletion of MTDH is a potentially novel avenue for effective cancer therapy. The microarray was performed on three biological triplicates as well as three experimental triplicates of stable knockdown and control cells. MTDH was knocked down using a shRNA.

2011-05-01 | E-GEOD-27828 | biostudies-arrayexpress

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