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Comparative analysis of glioblastoma initiating cells and patient-matched EPSC-derived neural stem cells as a discovery tool and drug matching strategy [Seq]

ABSTRACT: Malignant gliomas are the most common intrinsic brain tumours in adults and are associated with a very poor prognosis, which has not improved in the last 20 years. We show here that glioblastoma initiating cells (GIC) and syngeneic neural stem cells derived from enhanced pluripotent stem cells (iNSC) are a suitable novel pre-clinical pipeline to discover new patient-specific disease mechanisms and to identify druggable targets for personalised therapy.

ORGANISM(S): Mus musculus

PROVIDER: GSE154367 | GEO | 2021/09/17

REPOSITORIES: GEO

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Comparative analysis of glioblastoma initiating cells and patient-matched EPSC-derived neural stem cells as a discovery tool and drug matching strategy [RNA-Seq]

Project description:Malignant gliomas are the most common intrinsic brain tumours in adults and are associated with a very poor prognosis, which has not improved in the last 20 years. We show here that glioblastoma initiating cells (GIC) and syngeneic neural stem cells derived from enhanced pluripotent stem cells (iNSC) are a suitable novel pre-clinical pipeline to discover new patient-specific disease mechanisms and to identify druggable targets for personalised therapy.

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Comparative analysis of glioblastoma initiating cells and patient-matched EPSC-derived neural stem cells as a discovery tool and drug matching strategy

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Expression profiling of glioma initiating cells (GICs) in the sphere and differentiation conditions

Project description:Glioma initiating cells (GICs) are considered responsible for the therapeutic resistance and recurrence of malignant glioma. To clarify the molecular mechanism of GIC maintenance/differentiation, we established GIC clones from GBM patient tumors having the potential to differentiate into malignant gliomas in mouse intracranial xenograft, and established an in vitro glioma induction system by using serum stimulation. Upon the serum stimulation, the GIC spheres showed increased cellular proliferation, motility, filopodia/lameripodia formation and adhesion to the culture dishes. Simultaneously, the NSC marker proteins such as CD133 and Sox2 were down-regulated, and the astrocyte/glioma marker GFAP and the malignancy marker CD44 dramatically up-regulated. To identify genes/proteins whose expression changes dynamically during the differentiation of GICs into glioma cells, these GICs were subjected to DNA microarray/iTRAQ based integrated proteomics. Within 4 hours of tumor removal from GBM patients, tissues were subjected to GIC preparation. After successive cloning, total RNA from GIC clones (GIC03A and GIC03U) on day 2 or 7 of subculture in NSC medium with or without 10% FCS was subjected to the analysis with Affymetrix microarrays. Simultaneously, the proteins extracted from the same set of cells were subjected to LC-shot gun analyses using the 8-plex iTRAQ method. We sought to obtain the information of the common molecules that were up- or down-regulated during the GSC differentiation process, and functional targets for the early onset of GIC-associated glioma.

2013-01-26 | E-GEOD-43762 | biostudies-arrayexpress

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Project description:Glioma initiating/stem cells (GIC/GSC) are considered responsible for the therapeutic resistance and recurrence of malignant glioma. To clarify the molecular mechanism of GIC/GSC maintenance/differentiation, we established GIC/GSC clones, having the potential to differentiate into malignant gliomas, from glioblastoma patient’s tissues, and subjected to DNA microarray/iTRAQ based integrated proteomics. 21,857 mRNAs and 8,471 proteins were identified and integrated into a gene/protein expression analysis chart (iPEACH). The data integration and extraction of global proteins and mRNAs revealed that, during the GIC/GSC differentiation, cell adhesion molecules including integrin aV/ECMs and RAS-MAPK/PI3K signalings were significantly up-regulated, meanwhile, SOX2, CD133, and specific proteoglycans/synthetic-enzymes/metabolic pathways were obviously down-regulated. Among them, we focused proteoglycans and their synthetic-enzymes. GIC/GSC differentiation was significantly associated with the decrease of CSPG (CS-modified form) and dramatically induced by the CS-degradation enzyme which also induces the up-regulation of ERK-AKT signaling and GFAP without any other agents. Importantly, these differentiation processes were also associated with the interaction of CSPG (CS-unmodified form) and integrin-aV, and suppressed by integrin-inhibitors/CS administrations significantly. Combination treatments of a cancer-drug Temozolomide and these GIC/GSC-differentiation inhibitors suppressed glioma progression, increased the chemosensitivities, and led the longer survival of mouse xenograft-models. Functional integrated proteomics for the first time demonstrates that the GIC/GSC induces the specific proteoglycans to regulate GIC/GSC stemness/differentiation via the integlin signalings which may be a clinical target against malignant gliomas.

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