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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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE68995 | GEO | 2015/05/21

SECONDARY ACCESSION(S): PRJNA284494

REPOSITORIES: GEO

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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. 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.

2015-05-21 | E-GEOD-68995 | biostudies-arrayexpress

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

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

2015-05-21 | GSE68994 | 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

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Ptprz1-/- lung microvascular endothelial cell (LMVEC) Transcriptomes

Project description:Purpose: To compare NGS-derived transcriptome profiling (RNA-seq) between Wild Type and Ptprz1-/- LMVEC and identify transcripts that may be linked to the phenotypic differences observed. Methods: Total RNA from freshly cultured LMVEC was extracted using the NucleoSpin RNA Plus kit from Macherey-Nagel and the concentration and purity was assessed by Nanodrop and gel agarose 1% in TBE 0.5x. RNA from 3 independent fresh cell isolations from the Ptprz1+/+ and the Ptprz1-/- LMVEC was extracted and sent for RNAseq analysis. Novogene Co., Ltd performed the mRNA isolation, cDNA library synthesis and sequencing, and the bioinformatics analysis. Results: Pairwise comparison of gene expression of Ptprz1-/- RNA (3 samples) against Ptprz1+/+ RNA (3 samples) identified several transcripts as differentially expressed. Twenty-six genes were significantly changed (adj. p value <0.05), with 9 being upregulated and 17 downregulated. These genes are linked to angiogenesis and heart development and function. Conclusions: Our study represents the first transcriptomic analysis of Ptprz1-/- endothelial cells compared to the corresponding wild-type cells, generated by RNA-seq technology.

2022-01-19 | GSE161080 | GEO

Gene expression signatures for gata4/5/6 knocking down in zebrafish

Project description:Zebrafish gata4/5/6 are known to lie on the apex of the regulatory hierarchy in primitive myelopoiesis. However, little is known about the roles of microRNAs in this process. Performing microarray analysis on the expression changes of microRNAs in the gata4/5/6 knockdown embryos, we found that miR-210-5p is a novel regulator in zebrafish primitive myelopoiesis. To uncover the target genes of miR-210-5p to mediate its role in inhibiting zebrafish primitive myelopoiesis, we performed microarray analysis to identify differentially expressed genes in gata4/5/6 knockdown embryos.

2021-07-30 | GSE117958 | GEO

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

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

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