Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

44 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiles of PTPRZ1-knocking-down human glioblastoma stem cells [PrimeView]

ABSTRACT: Glioblastoma stem cells (GSCs), are at the apex of its cellular hierarchy and contribute to glioblastoma progression and tumor recurrence. Gene expression profiling is useful in determining the genome-wide gene expression changes based on the experimental purpose. In order to interrogate the downstream targets of PTPRZ1, we applied gene expression profiling approach to screen the altered genes that are responsible for the functional phenotype changes. The results will provide a cue for mechanical analysis with potential translational values. PTPRZ1-knocking down glioblastoma stem cells (GSCs) and control GSCs were used in this study. RNA were isolated using Primescript RT Master Mix (Takara). Profiling was established by applying PrimeView Affymetrix Human Gene Expression Array.

ORGANISM(S): Homo sapiens

SUBMITTER: Yu Shi

PROVIDER: E-GEOD-68995 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

PTPRZ1 disruption-mediated gene expression changes in human glioblastoma stem cells [HG-U133_Plus_2]

Project description:Glioblastoma is the most aggressive and lethal malignant brain tumor. Gene expression profiling is useful in determining the genome-wide gene expression changes based on the experimental purpose. In order to interrogate the downstream targets of PTPRZ1, we applied gene expression profiles to screen the altered genes that are responsible for the functional phenotype changes. The results will provide a cue for mechanical analysis with potential translational values. PTPRZ1-knocking down glioblastoma stem cells (GSCs) and control GSCs were used in this study. RNA were isolated using Primescript RT Master Mix (Takara). Profiling was established by applying Affymetrix GeneChip Human Genome U133 Plus 2.0 Array.

2015-05-21 | E-GEOD-68994 | biostudies-arrayexpress

Gene expression profiles of PTPRZ1-knocking-down human glioblastoma stem cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-05-21 | E-GEOD-69081 | biostudies-arrayexpress

Gene expression profiles of PTPRZ1-knocking-down human glioblastoma stem cells [PrimeView]

Project description:Glioblastoma stem cells (GSCs), are at the apex of its cellular hierarchy and contribute to glioblastoma progression and tumor recurrence. Gene expression profiling is useful in determining the genome-wide gene expression changes based on the experimental purpose. In order to interrogate the downstream targets of PTPRZ1, we applied gene expression profiling approach to screen the altered genes that are responsible for the functional phenotype changes. The results will provide a cue for mechanical analysis with potential translational values.

2015-05-21 | GSE68995 | GEO

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

Proteomic profiling of glioblastoma stem cells and their small extracellular vesicles

Project description:The heterogeneous nature of glioblastoma stem-like cells (GSCs) creates hurdles in developing effective therapies against glioblastoma, making it extremely difficult to eradicate. In this part of the project, we investigated the potential role of GSCs-derived small extracellular vesicles (sEVs) in glioblastoma heterogeneity, plasticity, and aggressiveness with the particular focus on their complexity in term of proteins. Proteome profiling of sEVs and their respective cell lines showed that GSCs-derived sEVs retain their subtype characteristics and are enriched in proteins playing a role in amino acids, carboxylic acids, organic acids transmembrane transport, and growth factor binding. In summary, we revealed the protein content of GSCs-derived sEVs and unveiled their potential contribution to tumor heterogeneity and critical cellular processes commonly deregulated in glioblastoma.

2024-05-21 | PXD036359 | Pride

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

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.

2020-08-25 | GSE156739 | GEO

Targeting EYA2 tyrosine phosphatase activity in glioblastoma stem cells induces mitotic catastrophe

Project description:Glioblastoma ranks among the most lethal of primary brain malignancies, with glioblastoma stem cells (GSCs) at the apex of tumor cellular hierarchies. Here, to discover novel therapeutic GSC targets, we interrogated gene expression profiles from GSCs, differentiated glioblastoma cells (DGCs), and neural stem cells (NSCs), revealing EYA2 as preferentially expressed by GSCs. Targeting EYA2 impaired GSC maintenance and induced cell cycle arrest, apoptosis, and loss of self-renewal. EYA2 displayed novel localization to centrosomes in GSCs, and EYA2 tyrosine (Tyr) phosphatase activity was essential for proper mitotic spindle assembly and survival of GSCs. Inhibition of the EYA2 Tyr phosphatase activity, via genetic or pharmacological means, mimicked EYA2 loss in GSCs in vitro and extended the survival of tumor-bearing mice. Supporting the clinical relevance of these findings, EYA2 portends poor patient prognosis in glioblastoma. Collectively, our data indicate that EYA2 phosphatase function plays selective critical roles in the growth and survival of GSCs, potentially offering a high therapeutic index for EYA2 inhibitors.

2021-09-25 | GSE135306 | GEO

Identification of novel BMP target genes in glioblastoma

Project description:It has been previously described that in glioblastoma (GBM), BMPs deplete the tumorigenic potential of glioblastoma stem cells (GSCs), promoting their differentiation towards the astrocytic lineage. To gain more insight on how BMPs regulate differentiation in GSCs, we are interested in identifying new BMP target genes in GBM cells. To this end, the patient derived glioblastoma cell lines U3031MG and U3034MG were stimulated or not with 30ng/ml BMP7 for 2 and 24 h, total RNA was isolated from three biological replicates per condition, and a microarray screen with the Affymetrix U133plus2 platform was performed.

2021-05-01 | E-MTAB-9811 | biostudies-arrayexpress

Transforming growth factor β (TGFβ) and BMP7 regulate glioblastoma stem cells differentiation status

Project description:Glioblastoma stem cells (GSCs) fate is controlled by environmental cues, among which cytokines play a crucial role. The transforming growth factor β (TGFβ) family signaling pathways controls GSCs. On one hand, TGFβ promotes cell proliferation in GBM, it induces the expression of platelet-derived growth factor-B (PDGFB). Moreover, TGFβ, via its signaling mediators Smad2/3, induces the expression of the cytokine leukemia inhibitory factor (LIF) and Sox4, which in turn enhances the expression of the stem cell transcription factor Sox2; this increases the self-renewal capacity of the GSCs and their stemness characteristics, and enhances the GSC tumor-initiating potential. On the other hand, Bone morphogenic proteins (BMPs) are known to promote GSC differentiation towards the astrocytic phenotype. To further understand which genes are regulated by TGFβ and BMP7 in GSCs we performed a microarray in the Affymetrix HTA2 platform in three different glioblastoma cell line, U2987, and two patient-derived glioblastoma stem cells, U3031MG and U3034MG, in the presence or absence of 5 ng/ml of TGFβ or 30 ng/ml BMP7 for 24 h, three biological replicates per condition.

2020-09-01 | E-MTAB-9076 | biostudies-arrayexpress

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data