This SuperSeries is composed of the SubSeries listed below.
Knockdown of NAT12/NAA30 reduces tumorigenic features of glioblastoma-initiating cells.
Specimen part, Treatment
View SamplesGene knockdown of NAT12/NAA30 led to decreased proliferation, sphere forming ability and mitochondrial hypoxia tolerance in the GSC T65 culture. Intracranial transplantation of these cells into SCID mice showed that the decreased NAT12/NAA30 expression correlated with the prolonged animal survival and reduced tumor size
Knockdown of NAT12/NAA30 reduces tumorigenic features of glioblastoma-initiating cells.
Specimen part, Treatment
View SamplesThis microarray contains expression data for two GBM tissue samples, four GSC cultures grown as spheres and one NFC culture grown as spheres
Knockdown of NAT12/NAA30 reduces tumorigenic features of glioblastoma-initiating cells.
Specimen part, Treatment
View SamplesGene expression profiles were assessed for vincristine-sensitive parental ovarian tumor cell line (SKOV3) and its highly vincristine-resistant derivative (SKVCR 2.0)
Genetic changes in the evolution of multidrug resistance for cultured human ovarian cancer cells.
No sample metadata fields
View SamplesThese arrays are used for various projects
DNA amplification is a ubiquitous mechanism of oncogene activation in lung and other cancers.
Sex, Age, Race
View SamplesGlioma cells are sensitized to the alkylator temozolomide after exposure to IFN-beta. In glioma-initiating cells (GIC), IFN-beta alone reduces clonogenicity. We investigated differentially expressed genes with or without IFN exposure in either longterm glioma cells or GIC.
Interferon-β induces loss of spherogenicity and overcomes therapy resistance of glioblastoma stem cells.
Specimen part, Cell line
View SamplesLysosomal cathepsins regulate an exquisite range of biological functions, and their deregulation is associated with inflammatory, metabolic and degenerative disease in humans. Here, we identified a key cell-intrinsic role for cathepsin B as a negative feedback regulator of lysosomal biogenesis and autophagy. Mice and macrophages lacking cathepsin B activity had increased resistance to the cytosolic bacterial pathogen Francisella novicida. Genetic deletion or pharmacological inhibition of cathepsin B downregulated mTOR activity and prevented cleavage of the lysosomal calcium channel TRPML1. These events drove transcription of lysosomal and autophagy genes via the transcription factor TFEB, which increased lysosomal biogenesis and activation of autophagy-initiation kinase ULK1 for clearance of the bacteria. Our results identified a fundamental biological function of cathepsin B in providing a checkpoint for homeostatic maintenance of lysosome population and basic recycling functions in the cell.
Cathepsin B modulates lysosomal biogenesis and host defense against Francisella novicida infection.
Specimen part
View SamplesRecent studies demonstrated that tumor cells with stem cell-like properties can be cultured from human glioblastomas by using conditions that select for the expansion of neural stem cells. We established glioblastoma stem-like (GS-) cell cultures from 9 different glioblastomas, 8 of which generated stably expandable cell lines. Analyzing GS-cell cultures, we discovered two clearly discernable phenotypes.
Glioblastoma-derived stem cell-enriched cultures form distinct subgroups according to molecular and phenotypic criteria.
No sample metadata fields
View SamplesIn this study, we explored the transcriptomic consequences of strong activation of the Notch pathway in embryonic human neural stem cells and in gliomas. For this we used a forced expression of the Notch intracellular domain (NICD).
Notch1 stimulation induces a vascularization switch with pericyte-like cell differentiation of glioblastoma stem cells.
Specimen part, Cell line
View SamplesRecent work using mouse models has revealed that mTORC2, which unlike mTORC1 is not acutely sensitive to rapamycin, plays a key role in the regulation of organismal physiology. The substrates and pathways regulated by mTORC2 are at present relatively unknown
Hepatic signaling by the mechanistic target of rapamycin complex 2 (mTORC2).
Sex, Specimen part, Treatment
View Samples