Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA227737 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We compared whole genome expression profiles of GSCs with normal human cortex, human neural stem cells (hNSC) from fetal cortex, glioblastoma (GBM) primary, and recurrent tumors to find GSC-specific plasma membrane transcripts. All of the expression profiles were batch normalized by a robust multichip average (RMA) algorithm using Geospiza GeneSifter (PerkinElmer) online microarray database and analysis software. The data was then exported into Microsoft Office Excel 2010 and organized for GSC transcripts with raw intensity values 10 fold or higher over normal brain, hNSCs, GBM primary and recurrent tumor samples. The reverse sorting algorithm was done to obtain downregulated GSC trascripts.
2013-11-14 | E-GEOD-51822 | biostudies-arrayexpress
Project description:We compared whole genome expression profiles of GSCs with normal human cortex, human neural stem cells (hNSC) from fetal cortex, glioblastoma (GBM) primary, and recurrent tumors to find GSC-specific plasma membrane transcripts.
2013-11-14 | GSE51822 | GEO
Project description:Expression data from glioblastoma stem cell clones (GSC)
| PRJNA200791 | ENA
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
Project description:<p>Glioblastoma (GBM) is a common and deadly form of brain tumor in adults. Dysregulated metabolism in GBM offers an opportunity to deploy metabolic interventions as precise therapeutic strategies. To identify the molecular drivers and the modalities by which different molecular subgroups of GBM exploit metabolic rewiring to sustain tumor progression, we interrogated the transcriptome, the metabolome, and the glycoproteome of human subgroup-specific GBM sphere-forming cells (GSC). L-fucose abundance and core fucosylation activation were elevated in mesenchymal (MES) compared with proneural GSCs; this pattern was retained in subgroup-specific xenografts and in subgroup-affiliated human patient samples. Genetic and pharmacological inhibition of core fucosylation significantly reduced tumor growth in MES GBM preclinical models. Liquid chromatography-mass spectrometry (LC-MS)-based glycoproteomic screening indicated that most MES-restricted core-fucosylated proteins are involved in therapeutically relevant GBM pathological processes, such as extracellular matrix interaction, cell adhesion, and integrin-mediated signaling. Selective L-fucose accumulation in MES GBMs was observed using preclinical minimally invasive PET, implicating this metabolite as a potential subgroup-restricted biomarker.Overall, these findings indicate that L-fucose pathway activation in MES GBM is a subgroup-specific dependency that could provide diagnostic markers and actionable therapeutic targets.</p><h4><strong>SIGNIFICANCE: </strong>Metabolic characterization of subgroup-specific glioblastoma (GBM) sphere-forming cells identifies the L-fucose pathway as a vulnerability restricted to mesenchymal GBM, disclosing a potential precision medicine strategy for targeting cancer metabolism.</h4><p><br></p><p><strong>Stem cell and cell line assays</strong> are reported in the current study <a href='https://www.ebi.ac.uk/metabolights/MTBLS4708' rel='noopener noreferrer' target='_blank'><strong>MTBLS4708</strong></a>.</p><p><strong>Xenograft assays</strong> are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS730' rel='noopener noreferrer' target='_blank'><strong>MTBLS730</strong></a>.</p>
2022-11-08 | MTBLS4708 | MetaboLights
Project description:<p>Glioblastoma (GBM) is a common and deadly form of brain tumor in adults. Dysregulated metabolism in GBM offers an opportunity to deploy metabolic interventions as precise therapeutic strategies. To identify the molecular drivers and the modalities by which different molecular subgroups of GBM exploit metabolic rewiring to sustain tumor progression, we interrogated the transcriptome, the metabolome, and the glycoproteome of human subgroup-specific GBM sphere-forming cells (GSC). L-fucose abundance and core fucosylation activation were elevated in mesenchymal (MES) compared with proneural GSCs; this pattern was retained in subgroup-specific xenografts and in subgroup-affiliated human patient samples. Genetic and pharmacological inhibition of core fucosylation significantly reduced tumor growth in MES GBM preclinical models. Liquid chromatography-mass spectrometry (LC-MS)-based glycoproteomic screening indicated that most MES-restricted core-fucosylated proteins are involved in therapeutically relevant GBM pathological processes, such as extracellular matrix interaction, cell adhesion, and integrin-mediated signaling. Selective L-fucose accumulation in MES GBMs was observed using preclinical minimally invasive PET, implicating this metabolite as a potential subgroup-restricted biomarker.Overall, these findings indicate that L-fucose pathway activation in MES GBM is a subgroup-specific dependency that could provide diagnostic markers and actionable therapeutic targets.</p><h4><strong>SIGNIFICANCE: </strong>Metabolic characterization of subgroup-specific glioblastoma (GBM) sphere-forming cells identifies the L-fucose pathway as a vulnerability restricted to mesenchymal GBM, disclosing a potential precision medicine strategy for targeting cancer metabolism.</h4><p><br></p><p><strong>Xenograft assays</strong> are reported in the current study <strong>MTBLS730</strong>.</p><p><strong>Stem cell and cell line assays</strong> are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS4708' rel='noopener noreferrer' target='_blank'><strong>MTBLS4708</strong></a>.</p>
2022-11-08 | MTBLS730 | MetaboLights
Project description:Gliomas are the most common type of primary malignant adult brain tumor. They appear to originate from neuroglial stem or progenitor cells, and are therapeutically challenging due to an invasive growth pattern and the absence of effective therapies. We have analyzed cellular, molecular and proteomic features and defined the therapeutic response profiles of four IDH1-wildtype glioma stem cell (GSC) cultures. All four GSC cultures were established from Grade IV glioblastoma (GBM) surgical resection tissue, can be continuously propagated and are highly enriched for stem/tumor repopulating cells. Integrated genomic and proteomic analysis of all four cultures was performed, together with use of a dual molecular bar-coding strategy to assess GSC population heterogeneity and the response to ionizing radiation. These well-characterized, bar-coded GSC cultures provide an experimentally tractable resource for investigating glioma biology, and to use to identify new and potentially more effective GBM therapies and treatment regimens.
2026-02-02 | PXD035886 | Pride
Project description:The persistence of Glioblastoma Stem-like Cells (GSCs) may account for the high lethality of glioblastoma patients. The GSC reservoir typically resides close to blood vessels, where these cells receive maintenance signals. Upon unfavorable conditions, GSCs escape these niches and spread by exploiting the pre-existing brain vasculature. In both scenarios, GSCs interact with the vascular interface, including the endothelial cells and their matrix. How cell adhesion encountered in their microenvironment serves GSC fate remains ill-defined. By combining ex vivo models, including decellularized matrices, cell co-culture, and organotypic slices, we identified that Junctional Adhesion Molecule C (JAMC) tethers GSCs to endothelial surface. Functionally, JAMC-/- GSCs exhibit an extended spreading on various endothelial-borne supports, with exacerbated invasive, migratory, and mesenchymal-like behaviors, that eventually eroded the survival of GSC tumor-bearing mice. Label-free quantitative proteomics next unveiled that JAMC deletion elicits an up-regulation of integrin expression, concurrent to a down-regulation of the integrin negative regulator, SHARPIN. Data mining of spatial transcriptomics confirmed the association between glioblastoma invasion and the expression pattern of JAMC. While JAMC may provide a retention signal in endothelial niches, the landscape of adhesion molecules anchoring GSCs to vascular surfaces may ultimately coordinate cell migration in defined glioblastoma territories.
2025-08-28 | PXD062679 | Pride
Project description:miRNAs are found to be extremely stable in extracellular fluids of mammals, such as blood plasma, serum, etc. The expression profiles of these circulating miRNAs have immense potential for use as novel minimally invasive markers in monitoring Dengue diseases progression.
2020-08-25 | GSE150623 | GEO
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