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Knockdown of NAT12/NAA30 decreases glioblastoma stem cell growth and tumorigenicity by regulating hypoxia response, p-MTOR (Ser2448) and p53 pathway

ABSTRACT: Gene knockdown of NAT12/NAA30 led to decreased proliferation, sphere forming ability and mitochondrial hypoxia tolerance in the GSC T65 culture. Intracranial transplantation of these cells into SCID mice showed that the decreased NAT12/NAA30 expression correlated with the prolonged animal survival and reduced tumor size

ORGANISM(S): Homo sapiens

PROVIDER: GSE60706 | GEO | 2015/11/23

SECONDARY ACCESSION(S): PRJNA259334

REPOSITORIES: GEO

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Knockdown of NAT12/NAA30 decreases glioblastoma stem cell growth and tumorigenicity by regulating hypoxia response, p-MTOR (Ser2448) and p53 pathway

Project description:Gene knockdown of NAT12/NAA30 led to decreased proliferation, sphere forming ability and mitochondrial hypoxia tolerance in the GSC T65 culture. Intracranial transplantation of these cells into SCID mice showed that the decreased NAT12/NAA30 expression correlated with the prolonged animal survival and reduced tumor size Total RNA isolated from GSC cultures featuring NAT12/NAA30 gene knock-down (shRNA) was compared to total RNA from non-silencing control GSC cultures (NS-shRNA).

2015-11-23 | E-GEOD-60706 | biostudies-arrayexpress

Targeting PBK/TOPK decreases growth and survival of glioblastoma stem cells in vitro and attenuates tumor growth in vivo

Project description:Gene knockdown of PBK led to decreased proliferation and sphere formation in the GSC cultures. Treatment of cells with different concentrations of HI-TOPK-032 almost completely abolished growth and proliferation and elicited a large increase in apoptosis Total RNA isolated from GSC cultures featuring PBK gene knock-down (shRNA) was compared to that from non-silencing control GSC cultures (NS-shRNA). Total RNA isolated from GSC cultures treated with PBK-inhibitor was compared to that from untreated GSC cultures.

2015-06-16 | E-GEOD-53800 | biostudies-arrayexpress

Serum Conditions Do Not Abolish The Tumorigenicity of Glioma Stem Cells

Project description:The subset of GBM patient samples gives rise to adherent cultures even in sphere culture conditions. Most samples in this subset are tumorigenic and exhibit a hybrid expression profile when tested with the marker panel. Cultures from these samples have a predominantly mesenchymal character based on substrate adherence, morphology, differentiation potential and gene expression. Total RNA isolated from glioblastoma stem cells (GSC) cultured as spheres was compared to that from adherent GSCs cultured in sphere culture conditions that exhibited both GSC and mesenchymal properties.

2016-07-21 | E-GEOD-74571 | biostudies-arrayexpress

Targeting PBK/TOPK decreases growth and survival of glioblastoma stem cells in vitro and attenuates tumor growth in vivo

2015-06-16 | GSE53800 | GEO

A Methylation Assay Predicts Response to Radiation Therapy in Patients with Glioblastoma

Project description:Genome wide DNA methylation profiling of glioma sphere-forming cells (GSC) derived from surgery specimens of glioblastoma patients.The Illumina Infinium 450K Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 450,000 CpGs in 12 GSC samples. Clonogeneic assays were used to detemine the radiation response of these 12 GSCs.

2016-10-06 | GSE75443 | GEO

Expression data from glioblastoma derived sphere lines, adherent cell lines and their original glioblastoma tumor

Project description:Glioblastoma (GBM) derived sphere lines and adherent cell lines are an important tool for research in basic and translational neuro-oncology. Documentation of their genetic identity has become a requirement for scientific journals and grant applications to exclude cross-contamination and misidentification that lead to misinterpretation of results. Here, we report expression data for 26 samples including 4 GBM derived sphere lines (4 x 3 replicates), 2 GBM derived sphere lines passaged through intracranial transplantation (2x 1), 2 adherent GBM derived cell lines (2 + 2 x 3 replicates), 4 corresponding glioblastoma tumors and 2 non-tumor brain tissues.

2017-09-27 | GSE104291 | GEO

Superenhancer-activation of KLHDC8A Drives Glioma Ciliation and Hedgehog signaling

Project description:Glioblastoma ranks among the most aggressive and lethal of all human cancers, with poor responses to all therapeutic modalities. Self-renewing, highly tumorigenic glioblastoma stem cells (GSCs) contribute to therapeutic resistance and maintain cellular heterogeneity. Identification of GSC vulnerabilities may provide novel therapeutic targets for treating glioblastoma. Here, we interrogated superenhancer landscapes of primary glioblastoma specimens and patient-derived GSCs, revealing a kelch domain-containing gene (KLHDC8A) with a previously unknown function as an epigenetically driven oncogene. Targeting KLHDC8A decreased GSC proliferation, reduced sphere formation, induced apoptosis, and impaired in vivo tumor growth. Transcription factor control circuitry analyses revealed that the master transcriptional regulator SOX2 contributes to KLHDC8A expression. Mechanistically, KLHDC8A functions in the assembly of primary cilia via interactions with Chaperonin-containing TCP1 (CCT) and establishes a platform for a critical stem-specific signaling node through the Hedgehog pathway. Furthermore, we identified that Hedgehog and Aurora B/C Kinase signaling are complementary in GSCs, and dual inhibition synergistically inhibits GSC proliferation. Collectively, superenhancers enrich for essential mediators of cellular identity and offer a novel regulatory mechanism whereby promotion of ciliogenesis establishes and maintains a core GSC signaling node via the Hedgehog pathway, potentially offering insights into therapeutic vulnerabilities for glioblastoma treatment.

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TGF-b-activated LncRNA LINC00115 is a critical regulator for glioma stem-like cell tumorigenicity

Project description:Long non-coding RNAs (lncRNAs) are critical regulators in cancer. However, the involvement of lncRNAs in TGF-beta-regulated tumorigenicity is still unclear. Here we identify TGF-beta-activated lncRNA LINC00115 as a critical regulator in glioma stem-like cell (GSC) self-renewal and tumorigenicity. LINC00115 is upregulated by TGF-beta, acts as a miRNA sponge and upregulates ZEB1 by competitively binding miR-200s, thereby enhancing ZEB1 signaling and GSC self-renewal.

2019-09-08 | GSE134595 | GEO

Identification and molecular characterization of distinct glioblastoma cancer stem cell populations

Project description:Malignant glioblastoma (GBM) is a highly aggressive brain tumor with a dismal prognosis and limited therapeutic options. Genomic profiling of GBM samples in the TCGA database has identified four molecular subtypes (Proneural, Neural, Classical and Mesenchymal), which may arise from different glioblastoma stem-like cell (GSC) populations. In the present study, we identify two GSC populations that produce GBM tumors by subcutaneous and intracranial injection with identical histological features. Gene expression analysis revealed that xenografts of GSCs grown as spheroid cultures had a Classical molecular subtype similar to that of bulk tumor cells. In contrast xenografts of GSCs grown as adherent cultures on laminin-coated plates expressed a Mesenchymal gene signature. Adherent GSC-derived xenografts had high STAT3 and ANGPTL4 expression as well as enrichment for stem cell markers, transcriptional networks and pro-angiogenic markers characteristic of the Mesenchymal subtype. Examination of clinical samples from GBM patients showed that STAT3 expression was directly correlated with ANGPTL4 expression, and that increased expression of these genes correlated with poor patient survival and performance. A pharmacological STAT3 inhibitor abrogated STAT3 binding to the ANGPTL4 promoter and exhibited anticancer activity in vivo. Taken together, we identified two distinct GSC populations that produce histologically identical tumors but with very different gene expression patterns, and a STAT3/ ANGPTL4 pathway in glioblastoma that may serve as a target for therapeutic intervention. 2 samples of each variable were analyzed. Cells were cultured under normal adherent conditon (Bulk tumor cells), non-adherent plates with stem cell medium (Sp-GSC) or laminin-coated plates with stem cell medium (Ad-GSC). Xenografts were generated in NSG mice by subcutaneous inoculation.

2015-07-01 | E-GEOD-65576 | biostudies-arrayexpress

Heterozygosity for hypoxia inducible factor 1alpha decreases the incidence of thymic lymphomas in a p53 mutant mouse model.

Project description:Hypoxia inducible factors (HIF) are critical mediators of the cellular response to decreased oxygen tension and are overexpressed in a number of tumors. Although HIF1alpha and HIF2alpha share a high degree of sequence homology, recent work has shown that the two alpha subunits can have contrasting and tissue-specific effects on tumor growth. To directly compare the role of each HIFalpha subunit in spontaneous tumorigenesis, we bred a mouse model of expanded HIF2alpha expression and Hif1alpha(+/-) mice to homozygotes for the R270H mutation in p53. Here, we report that p53(R270H/R270H) mice, which have not been previously described, develop a unique tumor spectrum relative to p53(R270H/-) mice, including a high incidence of thymic lymphomas. Heterozygosity for Hif1alpha significantly reduced the incidence of thymic lymphomas observed in this model. Moreover, reduced Hif1alpha levels correlated with decreased stabilization of activated Notch1 and expression of the Notch target genes, Dtx1 and Nrarp. These observations uncover a novel role for HIF1alpha in Notch pathway activation during T-cell lymphomagenesis.

| S-EPMC2707815 | biostudies-literature

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