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CN133 hampers tumor growth in patient-derived pediatric ependymoma models

ABSTRACT: HDACs are known to play crucial roles in cancer by deacetylating histones and non-histone substrates, leading to altered expression of genes involved in several cellular processes such as cell cycle control, apoptosis, DNA-damage response, angiogenesis, and autophagy, among othersto caracterize the transcriptomic changes induced by CN133 treatment on EPN cells, a microarray expression analysis of the EPP cell line treated with CN133 was performed

ORGANISM(S): Homo sapiens

PROVIDER: GSE139210 | GEO | 2019/10/22

REPOSITORIES: GEO

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Gene expression data from Brazilian pediatric ependymoma samples.

Project description:Ependymoma (EPN) is the third most common central nervous system (CNS) tumor in childhood and, recently, has been classified in nine robust molecular subgroups (Pajtler et al., 2015). However, molecular and clinical features of pediatric EPNs from Brazilian cohorts remain unexplored. Herein, we aimed to analyze the gene expression profile among three different molecular subgroups: ST-EPN-RELA, ST-EPN-YAP1 and PF-EPN-A.

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Histone serotonylation regulates ependymoma tumorigenesis through neurodevelopmental pathways

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RNA sequencing of posterior fossa ependymoma harboring 6q loss

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Sox9 directs divergent epigenomic states in brain tumor subtypes

Project description:Epigenetic dysregulation is a universal feature of cancer that results in altered patterns of gene expression that drive malignancy. Brain tumors exhibit subtype-specific epigenetic alterations, however the molecular mechanisms responsible for these diverse epigenetic states remain unclear. Here we show that the developmental transcription factor Sox9 differentially regulates epigenomic states in high-grade glioma (HGG) and ependymoma (EPN). These contrasting roles for Sox9 correspond with protein interactions with histone deacetylating complexes in HGG, and association with the Rela oncofusion in EPN. Together, our studies demonstrate how epigenomic states are differentially regulated in distinct subtypes of brain tumors, while revealing divergent roles for Sox9 in HGG and EPN tumorigenesis.

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Project description:Ependymoma (EPN) is a brain tumor commonly presenting in childhood that remains fatal in the majority of children. Intra-tumoral cellular heterogeneity in bulk tumor samples significantly confounds our understanding of EPN biology, impeding development of effective therapy. We used single-cell RNA sequencing to identify four neoplastic cell subpopulations in posterior fossa EPN patient samples that underlie traditional subgroup classification and harbor divergent lineage trajectories and clinical outcomes. Neoplastic subpopulations expressed gene signatures associated with normal ependyma, ependymoma, and mesenchymal phenotypes, consequently named ciliated (CEC), transportive (TEC), undifferentiated (UEC), and mesenchymal ependymoma cells (MEC). The abundance of EPN subpopulations as estimated by deconvolution of EPN bulk tumor transcriptomes showed that the ratio of MEC and CEC cell fractions dictated assignment to the two main classification subgroups in PFA. Longitudinal analysis revealed evolution of subpopulation fractions, notably MEC and CEC, which changed between presentation and recurrence. Outcome analyses demonstrated that a higher proportion of UEC or MEC subpopulations was associated with shorter survival, whereas CEC was associated with longer survival. Unsupervised pseudotime analysis revealed divergent subpopulation lineages. The first lineage conformed to a classic cancer stem cell trajectory where UEC progenitors differentiate sequentially to TECs and then CECs. In the second trajectory MECs arise from UECs via TECs, potentially in response to hypoxia-mediated cellular stress, a process that we recreated in vitro in a hypoxia treated EPN cell line. Our study reveals the existence of significant, unappreciated cellular heterogeneity in EPN and provides important resolution of EPN tumor biology.

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CN133, a Novel Brain-Penetrating Histone Deacetylase Inhibitor, Hampers Tumor Growth in Patient-Derived Pediatric Posterior Fossa Ependymoma Models.

Project description:Pediatric ependymoma (EPN) is a highly aggressive tumor of the central nervous system that remains incurable in 40% of cases. In children, the majority of cases develop in the posterior fossa and can be classified into two distinct molecular entities: EPN posterior fossa A (PF-EPN-A) and EPN posterior fossa B (PF-EPN-B). Patients with PF-EPN-A have poor outcome and are in demand of new therapies. In general, PF-EPN-A tumors show a balanced chromosome copy number profile and have no recurrent somatic nucleotide variants. However, these tumors present abundant epigenetic deregulations, thereby suggesting that epigenetic therapies could provide new opportunities for PF-EPN-A patients. In vitro epigenetic drug screening of 11 compounds showed that histone deacetylase inhibitors (HDACi) had the highest anti-proliferative activity in two PF-EPN-A patient-derived cell lines. Further screening of 5 new brain-penetrating HDACi showed that CN133 induced apoptosis in vitro, reduced tumor growth in vivo and significantly extended the survival of mice with orthotopically-implanted EPN tumors by modulation of the unfolded protein response, PI3K/Akt/mTOR signaling, and apoptotic pathways among others. In summary, our results provide solid preclinical evidence for the use of CN133 as a new therapeutic agent against PF-EPN-A tumors.

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Ependymoma subpopulation lineages underlie clinical classification and outcome (microarray data set)

Project description:Introduction: single-cell RNA sequencing identified multiple subpopulations in childhood posterior fossa ependymoma. The contribution of individual neoplastic subpopulations to bulk tumor transcriptome-based molecular classification and patient outcome was estimated by deconvolution in a cohort of clinically-annotated primary and recurrent EPN samples. The abundance of EPN subpopulations was estimated in primary EPN samples and showed that the ratio of subpopulation fractions dictated assignment to the two main transcriptomic classification subgroups in childhood posterior fossa ependymoma. Longitudinal analysis revealed that subpopulation fractions changed between presentation and recurrence. Outcome analyses demonstrated that a different proportions of subpopulations were associated with differential survival.

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Characterization of Two Novel Ependymoma Cell Lines with Chromosome 1q gain derived from Posterior Fossa Tumors of Childhood

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