Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA153229 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Eighteen independent neurospheres derived from patients affected by primary glioblastoma were grouped into “classical”, “mesenchymal” or “proneural” subtypes according to analysis of genetic lesions and gene expression profiling. Here we show that expression of the MET oncogene, encoding the tyrosine kinase receptor for HGF, associates with mesenchymal and proneural neurospheres (Met-pos-NS). Met expression is almost absent from classical neurospheres (Met-neg-NS), and mutually exclusive with amplification and expression of the EGF receptor gene. Met-pos-NS and Met-neg-NS display distinct growth factor requirements, differentiate along divergent pathways, and generate tumors with distinctive histological features. Met-pos-NS contain a variable percentage of Met positive (Methigh) and Met negative (Metneg) cells. After purification, only Methigh cells display clonogenic ability in vitro, and regenerate neurospheres containing both Methigh and Metneg cells. After in vivo transplantation, Methigh cells display highly enriched tumorigenic potential as compared with Metneg cells. At functional level, in Methigh cells, HGF concomitantly sustains proliferation, clonogenicity, expression of self-renewal markers, migration and invasion. These data show that Met is a functional marker of glioblastoma stem cells, and a candidate target for molecular diagnosis and therapy of a glioblastoma subset. 37 samples (17 replicate samples and 1 triplicate sample)
2012-10-05 | E-GEOD-36426 | biostudies-arrayexpress
Project description:Eighteen independent neurospheres derived from patients affected by primary glioblastoma were grouped into “classical”, “mesenchymal” or “proneural” subtypes according to analysis of genetic lesions and gene expression profiling. Here we show that expression of the MET oncogene, encoding the tyrosine kinase receptor for HGF, associates with mesenchymal and proneural neurospheres (Met-pos-NS). Met expression is almost absent from classical neurospheres (Met-neg-NS), and mutually exclusive with amplification and expression of the EGF receptor gene. Met-pos-NS and Met-neg-NS display distinct growth factor requirements, differentiate along divergent pathways, and generate tumors with distinctive histological features. Met-pos-NS contain a variable percentage of Met positive (Methigh) and Met negative (Metneg) cells. After purification, only Methigh cells display clonogenic ability in vitro, and regenerate neurospheres containing both Methigh and Metneg cells. After in vivo transplantation, Methigh cells display highly enriched tumorigenic potential as compared with Metneg cells. At functional level, in Methigh cells, HGF concomitantly sustains proliferation, clonogenicity, expression of self-renewal markers, migration and invasion. These data show that Met is a functional marker of glioblastoma stem cells, and a candidate target for molecular diagnosis and therapy of a glioblastoma subset.
2012-10-05 | GSE36426 | GEO
Project description:Cell plasticity is a crucial hallmark leading to cancer metastasis. Upregulation of Rho/ROCK pathway drives actomyosin contractility, protrusive forces and contributes to the occurrence of highly invasive amoeboid cells in tumors. Cancer stem cells are similarly associated with metastasis, but how these populations arise in tumors is not fully understood. Here we show that the novel oncogene RASSF1C drives mesenchymal to amoeboid transition and stem cell attributes in breast cancer cells. Mechanistically, RASSF1C activates Rho/ROCK via SRC mediated RhoGDI inhibition, resulting in generation of actomyosin contractility. Moreover, we demonstrate that amoeboid cells display the cancer stem cell markers CD133, ALDH1 and the pluripotent marker Nanog; are accompanied by higher invasive potential in vitro and in vivo; and employ extracellular vesicles to transfer the invasive phenotype to target cells and tissue. Importantly, the underlying RASSF1C driven biological processes concur to explain clinical data: namely, methylation of the RASSF1C promoter correlates with better survival in early stage breast cancer patients. Therefore, we propose the use of RASSF1 gene promoter methylation status as a biomarker for patient stratification.
2021-10-07 | PXD026226 | Pride
Project description:Wnt5a Drives The State Transition To An Invasive Phenotype In Human Glioblastoma Cancer Stem Cells
| PRJNA307251 | ENA
Project description:We studied MET-transformed human primary osteoblasts (MET-HOBs), which we previously turned into osteosarcoma cells by LV driven over-expression of MET oncogene. We obtained distinct MET transformed HOB clones derived from independent events of transgene integration. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays. Expression profiles of MET-HOBs and osteosarcoma cell lines were compared. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays
2013-02-28 | E-GEOD-28252 | biostudies-arrayexpress
Project description:We studied MET-transformed human primary osteoblasts (MET-HOBs), which we previously turned into osteosarcoma cells by LV driven over-expression of MET oncogene. We obtained distinct MET transformed HOB clones derived from independent events of transgene integration. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays. Expression profiles of MET-HOBs and parental HOBs were compared. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays
2013-02-28 | E-GEOD-28256 | biostudies-arrayexpress
Project description:The gene expression profiles of two groups of triplicate human glioblastoma (GBM) xenografts grown in immunodeficient rats were compared. The first group of xenografts was derived from a patient biopsy with Epidermal Growth Factor Receptor (EGFR) amplification which grows highly invasive and is independent of angiogenesis. The second group was obtained by introducing a dominant-negative EGFR mutant into the tumor cells, leading to a progression of the tumors to an angiogenic phenotype associated with a transition from a proneural to a mesenchymal GBM molecular subtype.
2017-07-05 | E-MTAB-4898 | biostudies-arrayexpress
Project description:We studied MET-transformed human primary osteoblasts (MET-HOBs), which we previously turned into osteosarcoma cells by LV driven over-expression of MET oncogene. We obtained distinct MET transformed HOB clones derived from independent events of transgene integration. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays. Expression profiles of MET-HOBs and parental HOBs were compared.
2013-02-28 | GSE28256 | GEO
Project description:We studied MET-transformed human primary osteoblasts (MET-HOBs), which we previously turned into osteosarcoma cells by LV driven over-expression of MET oncogene. We obtained distinct MET transformed HOB clones derived from independent events of transgene integration. To characterise the phenotype of the MET-HOB clones we used oligonucleotide microarrays. Expression profiles of MET-HOBs and osteosarcoma cell lines were compared.
2013-02-28 | GSE28252 | GEO
Project description:Epigenetic Activation of WNT5A Drives Glioblastoma Stem Cell Differentiation and Invasive Growth
| PRJNA338981 | ENA