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Expression data for developing a GE-HTS signature for neuroblastoma differentiation

ABSTRACT: Gene expression data from BE(2)-C cells treated in triplicate with either vehicle (DMSO), 5 M-NM- 2 > 3). Further investigation demonstrated that selective HDAC1/HDAC2 inhibition using compounds or RNA interference induced differentiation and decreased viability in neuroblastoma cell lines. Combined treatment with 13-cis retinoic acid augmented these effects and enhanced activation of retinoic acid signaling. Therefore, by applying a chemical genomic screening approach we identified selective HDAC1/HDAC2 inhibition as a strategy to induce neuroblastoma differentiation. BE(2)-C cells were treated in triplicate with either vehicle (DMSO), 5 M-NM-

ORGANISM(S): Homo sapiens

SUBMITTER: Kimberly Stegmaier

PROVIDER: E-GEOD-45587 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data for developing a GE-HTS signature for neuroblastoma differentiation

Project description:Gene expression data from BE(2)-C cells treated in triplicate with either vehicle (DMSO), 5 μM all-trans retinoic acid (ATRA), 1 mM valproic acid (VPA), or 5 μM ATRA + 1 mM VPA for 6, 24, or 72 hours. Genome-wide expression profiling was performed using Affymetrix U133A microarrays. While cytotoxic chemotherapy remains the hallmark of cancer treatment, intensive regimens fall short in many malignancies, including high-risk neuroblastoma. One alternative strategy is to therapeutically promote tumor differentiation. We created a gene expression signature to measure neuroblast maturation, adapted it to a high-throughput platform, and screened a diversity oriented synthesis-generated small-molecule library for differentiation inducers. We identified BRD8430, containing a nine-membered lactam, an ortho-amino anilide functionality, and three chiral centers, as a selective Class I histone deacetylase (HDAC) inhibitor (HDAC1 > 2 > 3). Further investigation demonstrated that selective HDAC1/HDAC2 inhibition using compounds or RNA interference induced differentiation and decreased viability in neuroblastoma cell lines. Combined treatment with 13-cis retinoic acid augmented these effects and enhanced activation of retinoic acid signaling. Therefore, by applying a chemical genomic screening approach we identified selective HDAC1/HDAC2 inhibition as a strategy to induce neuroblastoma differentiation.

2013-04-08 | GSE45587 | GEO

Co-targeting leukemia-initiating cells and leukemia bulk leads to disease eradication

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Nervous system development related gene expression regulation in the zebrafish embryo after exposure to valproic acid and retinoic acid: a genome wide approach

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Collateral lethality between HDAC1 and HDAC2 exploits cancer-specific NuRD complex vulnerabilities

Project description:Histone deacetylases (HDACs) have been widely pursued as targets for anti-cancer therapeutics. However, many of these targets are universally essential for cell survival, which may limit the therapeutic window that can be achieved by drug candidates. By examining large collections of CRISPR/Cas9-based essentiality screens, we discovered a genetic interaction between HDAC1 and HDAC2 wherein each paralog is synthetically lethal with hemizygous deletion of the other. This collateral synthetic lethality is caused by recurrent chromosomal translocations that occur in diverse solid and hematological malignancies, including neuroblastoma and multiple myeloma. Using genetic deletion or dTAG-mediated degradation, we show that HDAC2 disruption suppresses the growth of HDAC1-deficient neuroblastoma in vitro and in vivo. Mechanistically, we find that targeted degradation of HDAC2 in these cells prompts the degradation of several members of the nucleosome remodeling and deacetylase (NuRD) complex, leading to diminished chromatin accessibility at HDAC2/NuRD-bound sites of the genome and impaired control of enhancer-associated transcription. Furthermore, we reveal that several of the degraded NuRD complex subunits are dependencies in neuroblastoma and multiple myeloma, providing motivation to develop paralog-selective HDAC1 or HDAC2 degraders. Altogether, we identify HDAC1/2 collateral synthetic lethality as a new therapeutic target and reveal a novel mechanism for exploiting NuRD-associated cancer dependencies.

2023-06-11 | PXD034444 | Pride

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A novel miRNA fingerprint inversely associated with breast cancer progression in SKBR3 cells challenged with all-trans retinoic acid and lapatinib

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2015-04-30 | E-MTAB-3097 | biostudies-arrayexpress

RNA-seq of Primary Human Hepatocytes (PHH) exposed to Valproic Acid (VPA) for 3 days daily and 3 days daily exposure followed by 3 days washout.

Project description:Primary Human Hepatocytes (PHH) were exposed daily for 3 days to 15 mM VPA after which RNA was isolated. After terminating the VPA treatment, part of the cells were kept with medium for 3 days in order to investigate the eventual persistence of VPA-induced methylome changes. Identification of differentially expressed regions in the RNA was carried out by the RNA-seq method.

2018-02-23 | E-MTAB-5984 | biostudies-arrayexpress

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2024-01-24 | PXD046871 | Pride

Temporal Quantitative Proteomic Profiling of SH-SY5Y and IMR-32 Neuroblastoma Cells During All-trans Retinoic Acid-Induced Neuronal Differentiation

Project description:The human neuroblastoma cell lines SH-SY5Y and IMR-32 can be differentiated into neuron-like phenotypes through treatment with all-trans retinoic acid (ATRA). After differentiation, these cell lines are extensively utilized as in vitro models to study various aspects of neuronal cell biology. However, temporal and quantitative profiling of the proteome and phosphoproteome of SH-SY5Y and IMR-32 cells throughout ATRA-induced differentiation has been limited. Here, we performed relative quantification of the proteomes of SH-SY5Y and IMR-32 cells at multiple time points during ATRA-induced differentiation. The data presented serve as a valuable resource for investigating temporal protein and phosphoprotein abundance changes in SH-SY5Y and IMR-32 cells during ATRA-induced differentiation.

2024-01-24 | PXD046900 | Pride

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