Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA200791 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Glioblastoma stem cell (GSC) clones survived 500uM Temozolomide (TMZ) treatment
| PRJNA281656 | ENA
Project description:Expression data for minimally invasive glioblastoma stem-like cell (GSC) plasma membrane markers
| PRJNA227737 | ENA
Project description:Expression profiles of glioblastoma stem cells (GSC) treated with BMP7
| PRJNA281655 | ENA
Project description:Gene expression in glioblastoma (GBM) tissues, glioblastoma stem-like cell (GSC) cultures and neural foetal cell line (NFC)
| PRJNA259335 | ENA
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:Gene knockdown of PBK in the glioblastoma stem-like cell (GSC) culture T59
| PRJNA259333 | ENA
Project description:RNA-Seq of Glioblastoma stem-like cell (GSC) NSC11 with and without 2Gy irradiation.
| PRJNA371832 | ENA
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:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
2011-02-19 | GSE20463 | GEO