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LGR5 promotes tumorigenicity and invasion of glioblastoma stem-like cells and is a potential therapeutic target for a subset of glioblastoma patients [oeLGR5]

ABSTRACT: LGR5 promotes tumorigenicity and invasion of glioblastoma stem-like cells and is a potential therapeutic target for a subset of glioblastoma patients [oeLGR5]

PROVIDER: PRJNA476791 | ENA |

REPOSITORIES: ENA

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LGR5 promotes tumorigenicity and invasion of glioblastoma stem-like cells and is a potential therapeutic target for a subset of glioblastoma patients [oeLGR5]

Project description:Glioblastoma progression and recurrence are suggested to be derived by glioblastoma stem-like cells (GSCs). There is limited knowledge about the expression and therapy response of LGR5 in GSCs. We have investigated the role of LGR5 in glioblastoma by over-expression LGR5 using lentiviral vectors containing LGR5 cDNA (oeLGR5) or control (oeCTL).

2018-10-18 | GSE116012 | GEO

LGR5 promotes tumorigenicity and invasion of glioblastoma stem-like cells and is a potential therapeutic target for a subset of glioblastoma patients [shLGR5]

Project description:Glioblastoma progression and recurrence are suggested to be derived by glioblastoma stem-like cells (GSCs). There is limited knowledge about the expression and therapy response of LGR5 in GSCs. We have investigated the role of LGR5 in glioblastoma by knocking down LGR5 using short hairpin RNA targeting LGR5 mRNA (shLGR5) and non-target RNA (shNT) as control.

2018-10-18 | GSE109867 | GEO

LGR5 promotes tumorigenicity and invasion of glioblastoma stem-like cells and is a potential therapeutic target for a subset of glioblastoma patients [shLGR5]

Project description:LGR5 promotes tumorigenicity and invasion of glioblastoma stem-like cells and is a potential therapeutic target for a subset of glioblastoma patients [shLGR5]

| PRJNA432214 | ENA

Inhibition of Gli2 suppresses tumorigenicity in glioblastoma stem cells derived from a de novo murine brain cancer model

Project description:Prognosis of glioblastoma remains poor despite a great deal of research. In glioblastoma, the existence of glioblastoma stem cells (GSCs) has been shown, which are responsible for tumorigenesis, invasive capacity, and therapy resistance. One of cancer stem cell markers, Leucine-rich repeat-containing G-protein coupled receptor (Lgr5) plays a role in maintenance of GSCs, however, properties of the Lgr5 positive GSCs have not been fully understood. We applied the Sleeping-Beauty transposon-induced glioblastoma model to the Lgr5-GFP transgenic mice and sorted the GFP-positive cells from the neurosphere cultures derived from the mouse glioblastoma tissues. We found that the GFP-positive GSCs exhibited higher expression of Gli2 using a global gene expression analysis. Gli2 knockdown using lentiviral-mediated shRNA downregulates both the Hedgehog- and Wnt signaling pathway-related genes including Lgr5, suppresses tumor cell proliferation and invasion capacity, and induces apoptosis. Pharmacological Gli inhibition by GANT61 also suppresses tumor cell proliferation. Furthermore, the orthotopic transplantation model revealed that silencing of Gli2 suppresses tumorigenicity of GSCs in vivo. These findings demonstrate that Gli2 affects not only Hh pathway but also Wnt pathway and plays an important role in the GSC maintenance, suggesting that Gli2 may be a potential therapeutic target for glioblastoma treatment.

2020-08-20 | GSE156522 | GEO

Epigenetic regulation of MYC modulates glioblastoma tumorigenicity

Project description:One aspect of intra-tumoral heterogeneity in glioblastoma involves subpopulations of cells capable of self-renewal and indefinite propagation. Conceptually, this capacity is frequently treated as a static property. Here we provide data suggesting that tumorigenicity in glioblastomais a dynamic property that can be acquired or lost. Integrated expression analyses suggest that tumorigenicity is determined by the level of MYC expression relative to a threshold. Transitions between tumorigenic and non-tumorigenic cell states are associated with changes in histone modifications at the MYC locus, suggesting tumorigenicity is epigenetically regulated. To verify genomic stability at the nucleotide level, we tested whether subclones derived from single cells shared common Single-Nucleotide Polymorphisms (SNPs). Ten single cell-derived subclones of U87MG underwent SNP profiling by Affymetrix Human Mapping 250K Nsp arrays.

2014-03-28 | E-GEOD-56316 | biostudies-arrayexpress

Epigenetic regulation of MYC modulates glioblastoma tumorigenicity

2014-03-28 | GSE56316 | GEO

Horizontal mitochondrial transfer from microenvironment increases glioblastoma tumorigenicity

Project description:Horizontal mitochondrial transfer from microenvironment increases glioblastoma tumorigenicity

| PRJNA758703 | ENA

Inhibition of Gli2 suppresses tumorigenicity in glioblastoma stem cells derived from a de novo murine brain cancer model [Agilent-028005]

2020-08-25 | GSE156739 | GEO

Migration and invasion of 5 glioblastoma cell lines

Project description:Glioblastoma cells are characterized by a highly invasive behavior whose mechanisms are not yet understood. Using the wound healing and Boyden chamber assays we compared in the present study the migration and invasion abilities of 5 glioblastoma cell lines (DK-MG, GaMG, U87-MG, U373-MG, SNB19) differing in p53 and PTEN status. We also analyzed by Western blotting the expression of PTEN, p53, mTOR and several other marker proteins involved in cell adhesion, migration and invasion. Among 5 cell lines, GaMG cells exhibited the fastest rate of wound closure, whereas U87-MG cells showed the most rapid chemotactic migration in the Boyden chamber assay. In DK-MG and GaMG cells, F-actin mainly occurred in the numerous stress fibers spanning the cytoplasm, whereas U87-MG, U373-MG and SNB19 cells preferentially expressed F-actin in filopodia and lamellipodia. Moreover, the two glioblastoma lines mutated in both p53 and PTEN genes (U373-MG and SNB19) were found to exhibit the fastest invasion rates through the Matrigel matrix. Here, we performed a gene expression profiling of the five glioblastoma cell lines to examine the molecular framework of differences in invasive behavior to find possible targets for chemo- and radiation therapy.

2014-09-05 | E-GEOD-53124 | biostudies-arrayexpress

Stat5b inhibition blocks proliferation and tumorigenicity of glioblastoma stem cells derived from a de novo murine brain cancer model

Project description:Glioblastoma (GBM) is the most common and malignant type of brain cancer in adults with poor prognosis. GBM stem cells (GSCs) reside within niches in GBM tissues and contributes to recurrence and therapy resistance. Previous studies have shown that expression of leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5), a Wnt pathway-related stem cell marker, correlates with a poor prognosis in GBM, and its knockdown in GSCs induces apoptosis accompanied with downregulation of signal transducer and activator of transcription 5b (Stat5b). Here, we show that Stat5b co-localizes with Lgr5 in hypoxia-inducible factor 2α (Hif2α)-positive regions in GBM tissues. Functional analyses using GSCs derived from a murine de novo GBM model induced by oncogenic genes transduction using the Sleeping-Beauty transposon system revealed that expression of Stat5b was induced by culturing under hypoxia together with Lgr5, repressed by Hif2α knockdown, and reduced by Lgr5 knockdown or a Wnt/β-catenin signaling inhibitor ICG-001 treatment. Stat5b inhibition in the GSCs induced apoptosis and caused downregulation of Cyclin E2 resulted in blockade of entry into S-phase in the cell cycle. Disruption of Stat5b in an orthotopic transplantation model significantly prolongs event-free survival. These results suggest that Stat5b, regulated by hypoxia and the Wnt pathway, plays an important role in the maintenance and tumorigenicity of GSCs and may be a promising therapeutic molecular target to attack GSCs.

2021-10-17 | GSE185873 | GEO

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