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Gene expression profiling of histone deacetylase inhibition in triple-negative breast cancer

ABSTRACT: Analysis of changes in gene expression levels after after prolonged exposure of triple-negative breast cancer cell lines to low doses of Panobinostat (LBH589), a pan-histone deacetylase inhibitor.

ORGANISM(S): Homo sapiens

PROVIDER: GSE92910 | GEO | 2017/02/14

SECONDARY ACCESSION(S): PRJNA358776

REPOSITORIES: GEO

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Genome-wide DNA methylation maps of histone deacetylase inhibition in triple-negative breast cancer

Project description:Analysis of DNA methylation changes after prolonged exposure of triple-negative breast cancer cell lines to low doses of Panobinostat (LBH589), a pan-histone deacetylase inhibitor.

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Genome-wide maps of chromatin accessibility of histone deacetylase inhibition in triple-negative breast cancer

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HER3 targeting augments the efficacy of panobinostat in claudin-low triple-negative breast cancer cells

Project description:Patients with triple-negative breast cancer (TNBC) have a poor prognosis and high relapse rate due to limited therapeutic options. This study was conducted to determine the mechanisms of action of panobinostat, a pan-inhibitor of histone deacetylase (HDAC) and FDA-approved medication for multiple myeloma, in TNBC and to provide a rationale for effective drug combinations against this aggressive disease. RNA sequencing analyses of the claudin-low (CL) TNBC (MDA-MB-231) cells untreated or treated with panobinostat were performed to identify the differentially expressed genes. Adaptive alterations in gene expression were analyzed and validated in additional CL TNBC cells. Tumor xenograft models were used to test the in vivo antitumor activity of panobinostat alone or its combinations with gefitinib, an EGFR-tyrosine kinase inhibitor (TKI). Panobinostat potently inhibited proliferation and induced apoptosis in all TNBC cells tested. However, in CL TNBC cells, this HDAC inhibitor markedly enhanced expression of HER3, which interacted with EGFR to activate both receptors and Akt signaling pathways. Combinations of panobinostat and gefitinib synergistically suppressed CL TNBC cell proliferation and promoted apoptosis in vitro and in vivo. Upregulation of HER3 compromises the efficacy of panobinostat in CL TNBC. Inactivation of HER3 combined with panobinostat represents a practical approach to combat CL TNBC.

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Histone deacetylase inhibition in triple-negative breast cancer

Project description:Histone deacetylase inhibition in triple-negative breast cancer

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Aberrant chromatin acetylation in MLL-AF9 leukemia mediates the response to HDAC inhibition (microarray)

Project description:We investigated the response of acute myeloid cells (AML) expressing MLL-AF9 fusion gene to the pan-HDACi panobinostat (LBH589), and found that low conentrations of panobinostat lead to MLL-AF9 cell toxicity and rapid changes in gene expression. Human hematopoietic stem/progenitor cells (HSPC) expressing MLL-AF9 fusion protein (Wei et al, Cancer Cell 2008) were cultured with 30 nM panobinostat during 6 and 24 hours. The different gene expression between cells treated and untreated was studied by gene expression analysis. Three independent HSPC-MA9 clones were used, for each two replicates of cells after culture with 30 nM panobinostat for 6 and 24 hours and one untreated were used. A total of 16 samples were analyzed.

2015-03-01 | E-GEOD-54218 | biostudies-arrayexpress

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

Project description:This SuperSeries is composed of the following subset Series: GSE26789: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (ALL-B and ALL-T) GSE26790: 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) GSE26791: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (Illumina) GSE26792: The HDAC inhibitor panobinostat (LBH589) inhibits Acute Lymphoblastic leukemia (ALL) in vitro and in vivo in a new characterized human ALL mice model (SNP) Refer to individual Series

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Aberrant chromatin acetylation in MLL-AF9 leukemia mediates the response to HDAC inhibition (microarray)

2015-03-01 | GSE54218 | GEO

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2023-12-08 | MSV000093608 | MassIVE

RNAseq to investigate transcriptional changes in human MM cell lines due to panobinostat, 5-Azacytidine, panobinostat+5-Azacytidine or n-methyl-2-pyrroldine (NMP) treatments.

Project description:Purpose: We applied RNA sequencing technology for high-throughput analysis of transcriptional changes within human MM cell lines JJN3 and U266 due to individual and combination drug treatment. Methods: JJN3 and U266 cells were treated with pan-HDACi panbobinostat, DNMTi 5-Azacytidine, panobinostat+5-Azacytidine or NMP for 4h or 24h in triplicate and transcriptional changes assessed by RNAseq using Illumina HiSeq platform. Specifically, JJN3 cells were treated with 10nM panobinostat, 2.5µM 5-Azacytidine, panobinostat+5-Azacytidine (at given doses), or 10mM NMP. U266 cells were treated with 10nM panobinostat, 10µM 5-Azacytidine, panobinostat+5-Azacytidine (at given doses), or 10mM NMP. Results: We report unique and overlapping transcriptional signatures that lead to the induction of apoptosis in human MM cell lines in a cell-specific manner due to individual or combination treatments. Conclusions: A detailed analysis of differential transcriptional events in human MM cell lines due to HDACi, DNMTi, HDACi+DNMTi and NMP appear to define the molecular events leading to apoptosis and drug mechanism of action. We tested triplicate experiments at 4h and 24hr time points in JJN3 and U266 cell lines against vehicle control treated cells.

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Analysis of gene expression in human malignant rhabdoid cells following prolonged treatment with the histone deacetylase inhibitor, Panobinostat

Project description:We hypothesized that prolonged treatment of malignant rhabdoid tumor cells with low-dose HDACi will drive cellular differentiation. We assessed changes in gene expression following 21 days treatment with the HDACi, Panobinostat, versus a DMSO vehcile control in three human MRT cell lines. Total RNA obtained from three human malignant rhabdoid tumor cell lines (G401, SJSC, STM91-01) cultured for 21 days in the presence of low-dose Panobinostat was compared to 21-day treated DMSO control cells. All treatments and cell lines were performed in triplicate.

2016-03-01 | E-GEOD-76664 | biostudies-arrayexpress

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