Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The cellular origin of perivasuclar glioblastoma by scRNA-seq

ABSTRACT: Understanding the cellular origin and differentiation status of glioblastoma is critical to resolve the etiology of the disease. we profile control and genetically modified human brain perivasuclar fibroblasts by single cell RNA sequencing (scRNAseq). From this, we observed the potential tumorigenicity of brian perivascular fibroblasts.

ORGANISM(S): Homo sapiens

PROVIDER: GSE171287 | GEO | 2022/04/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The cellular origin and differentiation status of glioblastoma by scRNA-seq

Project description:Understanding the cellular origin and differentiation status of glioblastoma is critical to resolve the etiology of the disease. we profile 18 patient glioblastomas by single cell RNA sequencing (scRNAseq). From this, we uncovered two principal cell-of-origin relations. Each lineage displays unique directional differentiation trajectories and transcriptional cores from the naïve cell populations. Thus, glioblastoma is defined by robust cell lineage features which may provide insights into the cell origin of the diseases.

2022-04-19 | GSE159416 | GEO

glioblastoma single cell RNAseq

Project description:Understanding the cellular origin and differentiation status of glioblastoma is critical to resolve the etiology of the disease. we profile 18 patient glioblastomas by single cell RNA sequencing (scRNAseq). From this, we uncovered two principal cell-of-origin relations. Each lineage displays unique directional differentiation trajectories and transcriptional cores from the naÃƒÂ¯ve cell populations. Thus, glioblastoma is defined by robust cell lineage features which may provide insights into the cell origin of the diseases.

| EGAS00001006236 | EGA

Involvement of the microenvironment in the VC-Resist glioblastoma cells

Project description:In order to understand which molecular mechanisms are involved in radiation resistance and tumor propagation of glioblastoma, our laboratory has developed in-vitro models capable of mimicking the perivascular niche. Indeed, our laboratory hypothesizes that this niche is essential for glioblastoma cells to acquire a radioresistant character. That is why we are considering culturing our glioblastoma cells (GL261 cells) with the factors secreted by the perivascular niche (conditioned medium of mouse brain blood vessels) in order to study which phosphoproteins are activated in the presence of these factors. In parallel, a RNA sequencing analysis was carried out

2024-01-23 | PXD042606 | Pride

Single-cell RNA-seq characterization of glioblastoma

Project description:We investigated the tumor microenvironment of glioblastoma at the celluar level using 10x scRNAseq.

2023-01-31 | GSE224090 | GEO

Gene expression profiles of Glioblastoma stem cells in which ALK or pleiotrophin expression was suppressed.

Project description:Cancer stem cells are believed to be responsible for tumor initiation and development. Much current research on human brain tumors is focused on the stem-like properties of glioblastoma stem cells. Anaplastic lymphoma kinase (ALK) and its ligand pleiotrophin are required for maintaining the stem-like properties and tumorigenicity of glioblastoma stem cells. Human glioblastoma stem cells (GB2) were infected with a lentivirus expressing an shRNA targeting ALK or pleiotrophin.

2011-09-30 | E-GEOD-32482 | biostudies-arrayexpress

Epigenetic regulation of MYC modulates glioblastoma tumorigenicity

Project description:One aspect of intra-tumoral heterogeneity in glioblastoma involves subpopulations of cells capable of self-renewal and indefinite propagation. Conceptually, this capacity is frequently treated as a static property. Here we provide data suggesting that tumorigenicity in glioblastomais a dynamic property that can be acquired or lost. Integrated expression analyses suggest that tumorigenicity is determined by the level of MYC expression relative to a threshold. Transitions between tumorigenic and non-tumorigenic cell states are associated with changes in histone modifications at the MYC locus, suggesting tumorigenicity is epigenetically regulated. To verify genomic stability at the nucleotide level, we tested whether subclones derived from single cells shared common Single-Nucleotide Polymorphisms (SNPs). Ten single cell-derived subclones of U87MG underwent SNP profiling by Affymetrix Human Mapping 250K Nsp arrays.

2014-03-28 | E-GEOD-56316 | biostudies-arrayexpress

Epigenetic regulation of MYC modulates glioblastoma tumorigenicity

2014-03-28 | GSE56316 | GEO

DNA methylation profiling of glioblastoma cancer stem cells

Project description:Glioblastoma (GBM) is thought to be driven by a sub-population of cancer stem cells (CSCs) that self-renew and recapitulate tumor heterogeneity, yet remain poorly understood. Here we present a comparative epigenomic analysis of GBM CSCs that reveals widespread activation of genes normally held in check by Polycomb repressors. These activated targets include a large set of developmental transcription factors (TFs) whose coordinated activation is unique to the CSCs. We demonstrate that a critical factor in the set, ASCL1, activates Wnt signaling by repressing the negative regulator DKK1. We show that ASCL1 is essential for maintenance and in vivo tumorigenicity of GBM CSCs. Genomewide binding profiles for ASCL1 and the Wnt effector LEF1 provide mechanistic insight and suggest widespread interactions between the TF module and the signaling pathway. Our findings demonstrate regulatory connections between ASCL1, Wnt signaling and collaborating TFs that are essential for the maintenance and tumorigenicity of GBM CSCs. Epigenomic profiling of glioblastoma stem cells

2013-05-28 | E-GEOD-46015 | biostudies-arrayexpress

Horizontal mitochondrial transfer from microenvironment increases glioblastoma tumorigenicity

Project description:Horizontal mitochondrial transfer from microenvironment increases glioblastoma tumorigenicity

| PRJNA758703 | ENA

Changes in chromatin state reveal a central role for the transcription factor ARNT2, in the control of glioblastoma stem cell tumorigenicity

Project description:Although a growing body of evidence indicates that the phenotypic plasticity exhibited by glioblastoma cells plays a central role in tumor development and post-therapy recurrence, the master drivers of their aggressiveness remain elusive. Here we mapped the changes in the transcriptionally permissive (H3K4me3) and repressive (H3K27me3) epigenetic histone marks accompanying the repression of glioblastoma stem cells (GSC) tumorigenicity. Genes with changing marks delineated a network of transcription factors related to cancerous behavior, stem state, and neural development, which highlighted a previously unsuspected association between repression of ARNT2 and loss of cell tumorigenicity. Immunohistochemistry confirmed ARNT2 expression in cell sub-populations of patients’ glioblastoma. Its transcriptional repression was consistently found in non-tumorigenic glioblastoma cells, compared to tumorigenic cells. Moreover, ARNT2 expression correlated with a stem signature at both the tissue level within the tumor core and at the single cell level in the patients’ tumors. ARNT2 knockdown decreased expression of the transcription factors SOX9, POU3F2 and OLIG2 known promoters of glioblastoma cell tumorigenicity, and repressed GSC tumorigenic properties in vivo. Our results unveil ARNT2 as a master gene of the glioblastoma tumorigenic cell signature, located at a node of the transcription factor network controlling glioblastoma cell aggressiveness.

2018-02-23 | GSE98330 | 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