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Functional Identification of Critical Bmi1 target genes in Neural Progenitor and Malignant Glioma cells

ABSTRACT: Functional Identification of Critical Bmi1 target genes in Neural Progenitor and Malignant Glioma cells

PROVIDER: PRJNA148249 | ENA |

REPOSITORIES: ENA

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Functional Identification of Critical Bmi1 target genes in Neural Progenitor and Malignant Glioma cells

2013-05-21 | GSE33912 | GEO

Functional Identification of Critical Bmi1 target genes in Neural Progenitor and Malignant Glioma cells

Project description:In this study, we combined a genome-wide analysis of the Polycomb protein Bmi1 and an in vivo RNAi screening to identify critical targets whose repression in neural progenitor and Malignant Glioma cells enables normal and aberrant self-renewal. Bmi1 ChIP-sequencing generated in 2 primary adult mouse Neural Progenitor cell lines, 1 mouse astrocytic cell line, 1 mouse Glioma initiating cell line, and 1 mouse Glioma cell line. In human cell lines, Bmi1 ChIP-seq was performed for foetal Neural Progenitor Cells, and 2 Glioblastoma Stem-like cells. ChIP-seq for AP-1 in one Glioblastoma stem-like cell line. ChIP-sequencing were generated using either Illumina GxII or HiSeq. We have further performed RNA-seq of adult Ink4a/Arf -/-;BMI1or GFP dox-inducible shRNA mNPC with a doxycycline inducible shRNA targeting BMI1 or GFP (as control). These cells were either treated with doxyclyine for 48h to ablate BMI1 and GFP expression or further subjected to short-term differentiation using either BMP4 (10ng/ml or 50ng/ml for 3 or 6hrs), or FBS (1 or 10% for 3 or 6hrs). Additional mouse RNA-seq were performed in two biological replica of adult mouse brains (littermate) with either wild-type FVB background or BMI1 -/-. Finally, we performed RNA-seq in human Glioblastoma stem-like cells (most likely belonging to the mesenchymal GBM subtype) treated with BMP7, Arvanil and doxycycline or EtOH treated as ctrl.

2013-05-21 | E-GEOD-33912 | biostudies-arrayexpress

Functional Identification of Critical Bmi1 target genes in Neural Progenitor and Malignant Glioma cells

Project description: Not available

| S-ECPF-GEOD-33912 | biostudies-other

Modeling Malignant Progression in Glioma

Project description:Modeling Malignant Progression in Glioma

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Modeling Malignant Progression in Glioma

Project description:Modeling Malignant Progression in Glioma

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Modeling Malignant Progression in Glioma

Project description:Modeling Malignant Progression in Glioma

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Senescence induced by BMI1 inhibition is a therapeutic vulnerability in H3K27M-mutant DIPG

Project description:We studied the effect of BMI1 inhibition in diffuse intrinsic pontine glioma cells (DIPG). We reported the application of chromatin immunoprecipitation sequencing for high-thoughput profiling of BMI1 and H2AK119ub in diffuse intrinsic pontine glioma cells (DIPG) in response to BMI1 inhibition. We also performed bulk RNA sequencing of DIPG cells in response to pharmacological inhibition or knockdown of BMI1.

2020-10-22 | GSE140768 | GEO

Targeting Glioma Stem Cells through Combined BMI1 and EZH2 Inhibition [RNA-seq]

Project description:Glioblastomas are lethal cancers defined by angiogenesis and pseudopalisading necrosis. Here, we demonstrate that these features are associated with distinct transcriptional programs, with vascular regions showing a Proneural profile and hypoxic regions a Mesenchymal pattern. As these regions harbor glioma stem cells (GSCs), we investigated the epigenetic regulation of these two niches. Proneural, perivascular GSCs activated EZH2, whereas Mesenchymal GSCs in hypoxic regions expressed BMI1 protein, which promoted cellular survival under stress. Using both genetic and pharmacologic inhibition, we found that Proneural GSCs are selectively sensitive to EZH2 disruption, whereas Mesenchymal GSCs are sensitive to BMI1 inhibition. Given that glioblastomas contain both Proneural and Mesenchymal GSCs, combined EZH2 and BMI1 targeting proved more effective than either agent alone both in culture and in vivo, suggesting that strategies that simultaneously target multiple epigenetic regulators within glioblastomas may be necessary to overcome resistance to therapies caused by intratumoral heterogeneity.

2017-10-01 | GSE86237 | GEO

Genes differentially expressed between Bmi1-overexpressing and empty vector control neural stem/progenitor cells

Project description:Neural stem/progenitor cells were isolated from the lateral ventricle wall of 4-6 week-old CD1 mice and grown as neurospheres under low density culture conditions. Test cells were transduced with bicistronic retroviral constructs for the over-expression of Bmi1 together with eGFP, and control cells were transduced with an empty vector construct expressing eGFP only. To identify genes, which are regulated by BMI1 in neural stem/progenitor cells, the gene expression profiles of neurosphere cells over-expressing Bmi1 were compared empty vector control cells using Affymetrix Gene mouse ST1.0 arrays 3 independent Bmi1-overexpressing neurosphere cultures (test samples) were compared to 3 independent empty vector neurosphere cultures (control samples).

2016-06-01 | E-GEOD-70451 | biostudies-arrayexpress

Transformation of quiescent adult oligodendrocyte precursor cells into malignant glioma through a multi-step reactivation process

Project description:How malignant gliomas arise in a mature brain remains a mystery, hindering the development of preventive and therapeutic interventions. We previously showed that oligodendrocyte precursor cells (OPCs) can be transformed into glioma when mutations are introduced perinatally. However, adult OPCs rarely proliferate compared to their perinatal counterparts. Whether these relatively quiescent cells have the potential to transform is unknown, which is a critical question considering the late onset of human glioma. Additionally, the events taking place between initial mutation and a fully developed tumor mass (pre-malignant phase) are particularly poorly understood in glioma. Here we used a temporally controllable Cre transgene to delete p53 and NF1 specifically in adult OPCs, and demonstrated that these cells consistently give rise to malignant gliomas. To investigate the transforming process of quiescent adult OPCs, we then tracked these cells throughout the pre-malignant phase, which revealed a dynamic multi-step transformation, starting with rapid but transient hyper-proliferative reactivation, followed by a long period of dormancy, then final malignant transformation. Using pharmacological approaches, we discovered that mTOR signaling is critical for both the initial OPC reactivation step and late stage tumor cell proliferation, and thus might be a potential target for both glioma prevention and treatment. In summary, our results firmly establish the transforming potential of adult OPCs, and reveal an actionable multi-phasic reactivation process that turns slowly dividing OPCs into malignant gliomas. 44K Mouse Development Oligo Microarrays from Agilent Technologies were used for microarray analysis. For each experiment, total RNA was fluorescently labeled and hybridized directly against a common reference sample generated from the RNA pool of four WT P17 mouse brain neocortex.

2014-09-09 | E-GEOD-61282 | biostudies-arrayexpress

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