Project description:We cultured tumor cells from 22 GBM under medium conditions favoring the growth of neural stem cells. 11 out of 15 primary GBM contained a significant CD133+ subpopulation that comprised cells showing all hallmarks of neural stem cells. Cell lines derived from these CD133+ GBM showed a neurosphere-like, non-adherent growth pattern. In contrast, 4 out of 15 cell lines derived from primary GBM grew adherent in vitro and were driven by CD133- tumor cells that fulfilled stem cell criteria. In vivo, these GBM were characterized by a significantly lower proliferation index but similar GFAP staining as compared to CD133+ GBM. Gene arrays from 2x3 representative cells lines are given. Experiment Overall Design: Human glioblastoma cells cultured in DMEM supplemented with EGF, FGF, LIF, B27.
Project description:We cultured tumor cells from 22 GBM under medium conditions favoring the growth of neural stem cells. 11 out of 15 primary GBM contained a significant CD133+ subpopulation that comprised cells showing all hallmarks of neural stem cells. Cell lines derived from these CD133+ GBM showed a neurosphere-like, non-adherent growth pattern. In contrast, 4 out of 15 cell lines derived from primary GBM grew adherent in vitro and were driven by CD133- tumor cells that fulfilled stem cell criteria. In vivo, these GBM were characterized by a significantly lower proliferation index but similar GFAP staining as compared to CD133+ GBM. Gene arrays from 2x3 representative cells lines are given. Keywords: Cancer stem cell, CD133, glioblastoma
Project description:We have recently demonstrated that human paediatric mesenchymal stem cells can be reprogrammed toward a Ewing’s sarcoma family tumor (ESFT) cancer stem cell (CSC) phenotype by mechanisms that implicate microRNAs (miRNAs). Here, we show that the miRNA profile of ESFT CSC is shared by embryonic stem cells and CSC from divergent tumor types. We also provide evidence that the miRNA profile of ESFT CSC is the result of reversible disruption of TARBP2-dependent miRNA maturation. Restoration of TARBP2 activity and systemic delivery of synthetic forms of either of two of its targets, miRNA-143 or miRNA-145, inhibited ESFT CSC clonogenicity and tumor growth in vivo. Our observations suggest that CSC self-renewal and tumor initiation may depend on deregulation of TARBP2-dependent miRNA expression. 2 samples of primary Ewing sarcomas, divided into CD133+ and CD133- fractions. One sample of EWS-FLI1 expressing human pediatric mesenchymal stem cells, divided into CD133+ and CD133- fractions. One sample of STA-ET-8.2 cells, divided into CD133+ and CD133- fractions.
Project description:Pancreatic cancer stem cells (CSCs) have been described as CD24+/CD44+/EpCAM+ or CD133+ cells. However, no study has determined the co-expression of all of these markers in pancreatic ductal adenocarcinoma. Similarly to other combinations of CSC markers, CD24+/ CD44+/EpCAM+/CD133+ phenotype might more accurately identify true pancreatic CSCs. Therefore, we performed a detailed co-expression analysis of CD24, CD44, EpCAM, and CD133 in 3 cell lines derived from primary pancreatic ductal adenocarcinomas (PDACs). Gene expression profiling was applied in order to further investigate the observed differences in proportion of cells that co-expressed CSC markers among the cell lines.
Project description:We investigated in parallel the miRNome and proteome of the small EVs (sEVs) released by two different human GBM established cell lines and by GBM primary cancer stem cell (CSC) lines, to explore the role of sEVs in their different tumor behavior and capacities, and to assess whether these different EVs that coexist in the tumor burden are functionally interrelated, and/or may together target distinct cellular pathways that converge on the same biological goals
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.
Project description:The neural stem cell marker CD133 is reported to identify cells within glioblastoma (GBM) that can initiate neurosphere growth and tumor formation, however, instances of CD133- cells exhibiting similar properties have also been reported. Here, we show that some PTEN-deficient GBM tumors produce a series of CD133+ and CD133- self-renewing tumor-initiating cell types and provide evidence that these cell types constitute a lineage hierarchy. Our results show that the capacities for self-renewal and tumor initiation in GBM need not be restricted to a uniform population of stem-like cells, but can be shared by a lineage of self-renewing cell types expressing a range of markers of forebrain lineage. Keywords: Expression and copy number analysis of glioblastomas and neurosphere forming derivative cell lines of same.