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WNT pathway activation promotes phenotypic reprogramming of glioblastoma derived cells in zebrafish nervous system microenvironment

ABSTRACT: phenotypic reprogramming ability of teh zebtafish brain microenviroment on GBM derived cells controlled by the activation of endogenous Wnt pathway Class comparison between different time point of human GBM cells trasplanted into zebrafish

ORGANISM(S): Homo sapiens

SUBMITTER: silvia bresolin

PROVIDER: E-GEOD-25012 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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WNT pathway activation promotes phenotypic reprogramming of glioblastoma derived cells in zebrafish nervous system microenvironment

Project description:phenotypic reprogramming ability of teh zebtafish brain microenviroment on GBM derived cells controlled by the activation of endogenous Wnt pathway

2013-02-28 | GSE25012 | GEO

WNT pathway activation promotes phenotypic reprogramming of glioblastoma derived cells in zebrafish nervous system microenvironment

Project description:phenotypic reprogramming ability of teh zebtafish brain microenviroment on GBM derived cells controlled by the activation of endogenous Wnt pathway Class comparison between different time point of human GBM cells trasplanted into zebrafish

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Glioma stem cell treatment with MELK-signaling inhibitors

Project description:Glioblastoma multiforme (GBM) is a highly lethal brain tumor. Due to resistance to current therapies, patient prognosis remains poor and development of novel and effective GBM therapy is crucial. Glioma stem cells (GSCs) have gained attention as therapeutic target in GBM due to their relative resistance to current therapies and potent tumor-initiating ability. Recent studies including our own identified that the mitotic kinase, maternal embryonic leucine-zipper kinase (MELK), is highly expressed in GBM tissues, specifically in GSCs, and its expression is inversely correlated with the post-surgical survival period of GBM patients. In addition, patient-derived GSCs depend on MELK for their survival and growth both in vitro and in vivo. Here, we provide evidence that the kinase activity of MELK is essential for the action of MELK in GSCs and vital for GBM growth. We utilized in silico structure-based analysis for protein-compound interaction to predict that a recently identified small molecule, Compound 1 (C1), binds to the kinase-active site of MELK protein and eliminates MELK kinase activity in nanomolar concentrations. When treated with C1, GSCs undergo mitotic arrest and subsequent cellular apoptosis in vitro, a phenotype identical to that observed using MELK shRNA-mediated knockdown. C1 treatment strongly induces tumor cell apoptosis in slice cultures of GBM surgical specimens and attenuates growth of mouse intracranial tumors derived from GSCs in a dose-dependent manner. Lastly, C1 treatment sensitizes GSCs to radiation treatment. Collectively, these data indicate that targeting MELK kinase activity is a promising approach to attenuate GBM growth by eliminating GSCs in tumors. Microarray-based expression analysis of glioma stem cells treated with MELK-signaling inhibitors

2013-08-28 | E-GEOD-50227 | biostudies-arrayexpress

SEVERE CONSEQUENCES OF A HIGH-LIPID DIET INCLUDE HYDROGEN SULFIDE DYSFUNCTION AND DISEASE AGGRESSION IN GLIOBLASTOMA

Project description:Glioblastoma (GBM) remains among the deadliest of human malignancies, and the emergence of the cancer stem cell (CSC) phenotype represents a major challenge to durable treatment response. Because the environmental and lifestyle factors that impact CSC populations are not clear, we sought to understand the consequences of diet on CSC enrichment. We evaluated disease progression in mice fed an obesity-inducing high-fat diet (HFD) versus a low-fat, control diet. HFD resulted in hyper-aggressive disease accompanied by CSC enrichment and shortened survival. HFD drove intracerebral accumulation of saturated fats, which inhibited the production of the cysteine metabolite and gasotransmitter, hydrogen sulfide (H2S). H2S functions principally through protein S-sulfhydration and regulates multiple programs including bioenergetics and metabolism. Inhibition of H2S increased proliferation and chemotherapy resistance, whereas treatment with H2S donors led to death of cultured GBM cells and stasis of GBM tumors in vivo. GBM specimens present an overall reduction in protein S-sulfhydration, primarily associated with proteins regulating cellular metabolism. These findings provide new evidence that diet modifiable H2S signaling serves to suppress GBM by restricting metabolic fitness, while its loss triggers CSC enrichment and disease acceleration. Interventions augmenting H2S bioavailability concurrent with GBM standard of care may improve outcomes for GBM patients.

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Project description:Using induced pluripotent stem cell (iPSC) technology, we reprogrammed GBM derived cells (GBM-DCs) into embryonic-like cells termed as induced core-GSCs (ic-GSCs). The aim of this experiment was to characterize the DNA methylation profile of ic-GSCs using the Infinium MethylationEPIC array BeadChip (850K, Illumina). For this experiment, we selected three biological replicates of GBM-DCs (GBM-DC1, GBM-DC2 and GBM-DC3) and three independent clonal lines of ic-GSCs (ic-GSC#1, ic-GSC#3 and ic-GSC#7).

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Gene expression profiling of core glioma stem cells: a novel glioblastoma cell population with diminished antigen presentation

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GBM brain tumors

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Glioblastoma serum biomarkers identification by iTRAQ

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2019-03-04 | PXD012207 | Pride

Annexin 2A sustains glioblastoma cell dissemination and proliferation affecting patient prognosis

Project description:Glioblastoma (GBM) is the most devastating tumour of the brain, endowed with a fatal prognosis. Indeed, the complete eradication of cancer cell disseminated outside the GBM mass still remains a crucial issue. Given the reported strong association existing between Annexin 2A (ANXA2) expression and cell dissemination in many cancers, we evaluated the effects exerted by the modulation of ANXA2 levels in GBM cells and assessed its potential in predicting patient outcome. Here, we show that expression of ANXA2 positively correlates with metastatic gene signatures and demonstrates to be prognostic by itself. Indeed, we prove that ANXA2 is involved in cell migration, invasion, cytoskeletal remodeling and proliferation in GBM cells. Moreover, we were able to construct a gene signature representative of ANXA2 inhibition, which showed a significant prognostic potential in different GBM patient cohorts. In this study, we demonstrate that ANXA2 acts at multiple levels in determining the disseminating and aggressive behaviour of GBM tumours. In particular, we clearly show that ANXA2 is involved in determining a migrating and disseminating phenotype of GBM cells, in controlling specific cell cycle checkpoints and a cytoskeletal remodeling associated to cell movement. These data sustain the potential of ANXA2 as a possible target and strong prognostic factor in the future management of GBM patients. Gene expression was measured on Affymetrix in 4 independent experiments of primary GBM cells treated with an ANXA2 neutralizing antibody

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