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RNA-sequencing analysis in human glioma stem cell

ABSTRACT: Glioblastomas show heterogeneous histological features. These distinct phenotypic states are thought to be associated with the presence of glioma stem cells (GSCs), which are highly tumorigenic and self-renewing sub-population of tumor cells that have different functional characteristics. To investigate Glioblastomas (GBMs) show heterogeneous histological features. These distinct phenotypic states are thought to be originated by the glioma stem cells (GSCs), which are highly tumorigenic and self-renewing sub-population of tumor cells. Notch signaling has been shown to be important for maintenance of GSC population both in vitro and in vivo. A recent study showed that NOTCH -triggered oncogenic activity can be due to not only its ability to regulate coding genes but also long non-coding RNAs (lncRNAs). Here, we investigated the molecular effects of lncRNA in GSC, whose expression is induced by Notch signaling. We searched for downregulated lncRNAs in GSCs by treatment of small interfering RNA (siRNA) targeting Notch1 and JAG1 (si-Notch1 and si-JAG1).

ORGANISM(S): Homo sapiens

PROVIDER: GSE86348 | GEO | 2016/11/23

SECONDARY ACCESSION(S): PRJNA341490

REPOSITORIES: GEO

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Analysis of Notch-regulated lncRNA in human glioma stem cell

Project description:Glioblastomas show heterogeneous histological features. These distinct phenotypic states are thought to be associated with the presence of glioma stem cells (GSCs), which are highly tumorigenic and self-renewing sub-population of tumor cells that have different functional characteristics. To investigate Glioblastomas (GBMs) show heterogeneous histological features. These distinct phenotypic states are thought to be originated by the glioma stem cells (GSCs), which are highly tumorigenic and self-renewing sub-population of tumor cells. Notch signaling has been shown to be important for maintenance of GSC population both in vitro and in vivo. A recent study showed that NOTCH -triggered oncogenic activity can be due to not only its ability to regulate coding genes but also long non-coding RNAs (lncRNAs). Here, we investigated the molecular effects of lncRNA in GSC, whose expression is induced by Notch signaling. We searched for downregulated lncRNAs in GSCs by treatment of small interfering RNA (siRNA) targeting Notch1 and JAG1 (si-Notch1 and si-JAG1) and γ-secretase inhibitors (N-S-phenyl-glycine-t-butyl ester (DAPT) and RO4929097) using SurePrint G3 Human GE 8×60K array slides (G4851B, Agilent Technologies).gene expression profiling in GSC, we have performed microarray experiment using Agilent Whole Human Genome Oligo Microarrays (G4112F).

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Project description:It is becoming better understood that radiation resistance in glioblastomas (GBMs) may be secondary to a self-renewing subpopulation of cells in the bulk tumor that form neurospheres in culture. This population has been referred to as Glioma stem cells (GSCs). One of the limitations regarding the use of GSCs is that these studies require fresh tumor biopsy samples obtained from patients, and can be extremely difficult to culture, propagate, and perform treatment-response assays. This report describes the generation of a self-renewing population of GSCs derived from commercially available U87 cells using NOD-SCID mice as carrier. The tumors were dissociated to obtain GSCs that demonstrate stem-like properties and high degree of chemo and radiation resistance. Pathological analysis of tumors obtained using GSCs exhibit all the histological hallmarks of human GBMs which is quite uncommon in GBM rodent models and hence could serve as a better model for pre-clinical study. We have shown that MGH87GSCs have an enhanced tumorogenicity than parental U87 and about 500 cells are sufficient to form tumors. To understand the transcriptome and accompanied proteome better, we explored the gene expression profiles of MGH87GSC and U87. We have shown that these GSCs are plastic like stem cells and can be directed towards a particular progeny within neural lineage by providing suitable growth factor. Our objective was to understand the genetic and biochemical mechanisms that control the self-renewal phenotype, asymmetric subdivision, chemo and radiation resistance and the role of the GSC niche in regulating the biological properties of GSC. Through this model we anticipate to devise therapeutic strategies to target this sub population of GSCs within GBMs to eradicate treatment resistance and tumor recurrence.

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Genome variation profiling of Glioma Stem Cell lines

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Project description:Glioblastoma (GBM) is a lethal brain cancer composed of heterogeneous cellular populations including glioma stem cells (GSCs) and their progeny differentiated non-stem glioma cells (NSGCs). Although accumulating evidence points out the significance of GSCs for tumour initiation and propagation, the roles of NSGCs remain elusive. Here we demonstrate that, when patient-derived GSCs in GBM tumours undergo differentiation with diminished telomerase activity and shortened telomeres, they subsequently become senescent phenotype, thereby secreting angiogenesis-related proteins, including vascular endothelial growth factors. Interestingly, these secreted factors from senescent NSGCs promote proliferation of human umbilical vein endothelial cells and tumorigenic potentials of GSCs in immunocompromised mice. These experimental data are likely clinically-relevant, since immunohistochemistry of both patient tumours of GBM and the patient GSC-derived mouse xenografted tumours detected tumour cells that express a set of markers for the senescence phenotype. Collectively, our data suggest that the inter-cellular signals from senescent NSGCs promote GBM tumour angiogenesis thereby increasing malignant progression of GBM. We monitored gene expression profiling in GSC, differentiated NSGC (GSC at day7 after serum exposure), and senescent NSGC (GSC at day30 after serum exposure) of GBM146 and GBM157.

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Contribution of microRNA-1275 to Claudin11 protein suppression via a polycomb-mediated silencing mechanism in human glioma stem-like cells.

Project description:Glioblastomas show heterogeneous histological features, in which tumor cells show distinct phenotypic states that confer different functional attributes. This functional and morphological heterogeneity characterizes aggressive glioblastoma; however, molecular mechanisms underlying the heterogeneity are poorly understood. Glioma stem-like cells (GSCs) are considered able to aberrantly differentiate into diverse cell types and may contribute the establishment of tumor heterogeneity. Using the GSC model, we investigated the differentially expressed microRNAs(miRNAs) and associated epigenetic mechanism that regulate the differentiation of GSCs. MiRNA-microarray showed that 13 and 34 miRNAs were commonly upregulated and downregulated in two independent GSC lines during differentiation, respectively. Among those miRNAs, quantitative-PCR analysis showed that miR-1275 was consistently downregulated during the GSC differentiation along with the upregulation of its target, CLDN11, a marker of oligodendroglial-lineage differentiation. Compellingly, inhibition of miR-1275 with specific antisense oligonucleotide (anti-miR-1275) in GSC increased the expression of CLDN11, together with significant growth suppression. Epigenetic analysis revealed that gain of histone H3 lysine 27 trimethylation (H3K27me3) and loss of H3K9Ac in the pri-miR-1275 promoter were closely associated with the miR-1275 expression. Treatment of 3-Dezaneplanocin-A, an inhibitor of H3K27 methyltransferase, impaired the GSC differentiation in parallel with sustained miR-1275 expression. Our results illuminated the epigenetic regulatory pathways of miR-1275 closely associated with oligodendroglial differentiation, which may contribute to the tissue heterogeneity formation of glioblastomas. Inhibition of miR-1275 induces the GSC differentiation and suppresses tumor cell proliferation, miR-1275 may be a potential therapeutic target for glioblastomas.

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