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A reference collection of cell line and xenograft models of proneural, classical and mesenchymal GBM [cell line]

ABSTRACT: Low-passage, serum-free cell lines cultured from patient tumour tissue are the gold-standard for preclinical studies and cellular investigations of glioblastoma (GBM) biology, yet entrenched, poorly-representative cell line models are still widely used, compromising the significance of much GBM research. We submit that greater adoption of these critical resources will be promoted by the provision of a suitably-sized, meaningfully-described reference collection along with appropriate tools for working with them. Consequently, we present a curated panel of 12 readily-usable, genetically-diverse, tumourigenic, patient-derived, low-passage, serum-free cell lines representing the spectrum of molecular subtypes of IDH-wildtype GBM along with their detailed phenotypic characterisation and a bespoke set of lentiviral plasmids for bioluminescent/fluorescent labelling, gene expression and CRISPR/Cas9-mediated gene inactivation. The cell lines and all accompanying data are readily-accessible via a single website, Q-Cell (qimrberghofer.edu.au/q-cell/) and all plasmids are available from Addgene. These resources should prove valuable to investigators seeking readily-usable, well-characterised, clinically-relevant, gold-standard models of GBM. Gene expression in 12 matched patient tumour / derived cell line / resultant xenograft samples was measured using Illumina HumanHT-12_V4_0_R2_15002873_B direct hybridisation beadchips.

ORGANISM(S): Homo sapiens

PROVIDER: GSE118790 | GEO | 2018/08/21

REPOSITORIES: GEO

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A reference collection of cell line and xenograft models of proneural, classical and mesenchymal GBM [xenograft]

Project description:Low-passage, serum-free cell lines cultured from patient tumour tissue are the gold-standard for preclinical studies and cellular investigations of glioblastoma (GBM) biology, yet entrenched, poorly-representative cell line models are still widely used, compromising the significance of much GBM research. We submit that greater adoption of these critical resources will be promoted by the provision of a suitably-sized, meaningfully-described reference collection along with appropriate tools for working with them. Consequently, we present a curated panel of 12 readily-usable, genetically-diverse, tumourigenic, patient-derived, low-passage, serum-free cell lines representing the spectrum of molecular subtypes of IDH-wildtype GBM along with their detailed phenotypic characterisation and a bespoke set of lentiviral plasmids for bioluminescent/fluorescent labelling, gene expression and CRISPR/Cas9-mediated gene inactivation. The cell lines and all accompanying data are readily-accessible via a single website, Q-Cell (qimrberghofer.edu.au/q-cell/) and all plasmids are available from Addgene. These resources should prove valuable to investigators seeking readily-usable, well-characterised, clinically-relevant, gold-standard models of GBM. Gene expression in 12 matched patient tumour / derived cell line / resultant xenograft samples was measured using Illumina HumanHT-12_V4_0_R2_15002873_B direct hybridisation beadchips.

2018-08-21 | GSE118792 | GEO

A reference collection of cell line and xenograft models of proneural, classical and mesenchymal GBM [tumor tissue]

2018-08-21 | GSE118791 | GEO

Gene expression data of GBM146 and GBM157 at day0, 7, 30 after serum exposure

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.

2015-10-24 | E-GEOD-74304 | biostudies-arrayexpress

Gene expression data of GBM146 and GBM157 at day0, 7, 30 after serum exposure

2015-10-24 | GSE74304 | GEO

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

2016-07-24 | E-GEOD-76786 | biostudies-arrayexpress

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

2016-07-24 | GSE76786 | GEO

Single cell gene expression profiling of slow cycling and actively dividing mouse glioblastoma (GBM) cells isolated based on H2B-GFP label retention.

Project description:A slow cycling, dormant cell state is thought to contribute to the therapeutic resistance of GBM tumour cells, yet not much is known about the biology of this slow-cycling cell population in GBM. By using somatic mouse model of GBM, combined with the inducible H2B-GFP label retention system, we isolated dormant tumour cells from their in vivo niches, and characterised them by single cell RNA sequencing.

2023-04-03 | GSE228785 | GEO

Project description:Mayo Clinic GBM PDX National Resources

| PRJNA543854 | ENA

Tumour-associated microglia/macrophages in Glioblastoma are heterogenous and display higher immunological reactivity under aconitate decarboxylase 1 deficiency

Project description:In Glioblastoma (GBM), tumour-associated microglia/macrophages (TAMs) represent the most abundant cells of the stromal compartment contributing to tumour immune escape mechanisms. Thus, strategies targeting TAMs are emerging as promising objectives for immunotherapy. However, TAMs heterogeneity is only starting to emerge and little is known about their contribution to GBM progression. Here, we comprehensively study the molecular changes of TAMs in the GL261 GBM mouse model by single-cell RNA-sequencing across GBM progression and in the absence of Acod1/Irg1, a key gene involved in macrophage metabolic reprogramming. We identify distinct TAM profiles, mainly based on their ontogeny, which recapitulate microglia- versus macrophage-like features showing key transcriptional differences and rapidly adapting along GBM stages. Notably, we uncover a decreased antigen-presenting cell signature in TAMs along tumour progression that is less prominent in Acod1/Irg1-deficient mice. Overall, our results provide insights into TAMs heterogeneity and highlight a potential role for Acod1/Irg1 in TAMs polarization along GBM progression.

2020-09-16 | GSE158016 | GEO

Inhibition of glioblastoma cell proliferation and invasion by the choline-kinase inhibitor JAS239 varies with cell type and hypoxia.

Project description:<h4><strong>BACKGROUND:</strong> Elevated choline kinase alpha (ChoK) is observed in most solid tumours including glioblastomas (GBM), yet until recently, inhibitors of ChoK have demonstrated limited efficacy in GBM models. Given that hypoxia is associated with GBM therapy resistance, we hypothesised that tumour hypoxia could be responsible for such limitations. We therefore evaluated in GBM cells, the effect of hypoxia on the function of JAS239, a potent ChoK inhibitor.</h4><h4><strong>METHODS:</strong> Rodent (F98 and 9L) and human (U-87 MG and U-251 MG) GBM cell lines were subjected to 72 hours of hypoxia conditioning and treated with JAS239 for 24 hours. NMR metabolomic measurements and analyses were performed to evaluate the signalling pathways involved. In addition, cell proliferation, cell cycle progression and cell invasion were measured in cell monolayers and 3D spheroids, with or without JAS239 treatment in normoxic or hypoxic cells to assess how hypoxia affects JAS239 function.</h4><h4><strong>RESULTS:</strong> Hypoxia and JAS239 treatment led to significant changes in the cellular metabolic pathways, specifically the phospholipid and glycolytic pathways associated with a reduction in cell proliferation via induced cell cycle arrest. Interestingly, JAS239 also impaired GBM invasion. However, JAS239 effects were variable depending on the cell line, reflecting the inherent heterogeneity observed in GBMs.</h4><h4><strong>CONCLUSION:</strong> Our findings indicate that JAS239 and hypoxia can deregulate cellular metabolism, inhibit proliferation and alter cell invasion. These results may be useful for the design of new therapeutic strategies based on ChoK inhibition that can act on multiple pro-tumorigenic features.</h4>

2024-06-18 | MTBLS6212 | MetaboLights

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