Project description:Glioblastoma is the most aggressive and lethal malignant brain tumor. Gene expression profiling is useful in determining the genome-wide gene expression changes based on the experimental purpose. In order to interrogate the downstream targets of PTPRZ1, we applied gene expression profiles to screen the altered genes that are responsible for the functional phenotype changes. The results will provide a cue for mechanical analysis with potential translational values. PTPRZ1-knocking down glioblastoma stem cells (GSCs) and control GSCs were used in this study. RNA were isolated using Primescript RT Master Mix (Takara). Profiling was established by applying Affymetrix GeneChip Human Genome U133 Plus 2.0 Array.
Project description:Glioblastoma stem cells (GSCs), are at the apex of its cellular hierarchy and contribute to glioblastoma progression and tumor recurrence. Gene expression profiling is useful in determining the genome-wide gene expression changes based on the experimental purpose. In order to interrogate the downstream targets of PTPRZ1, we applied gene expression profiling approach to screen the altered genes that are responsible for the functional phenotype changes. The results will provide a cue for mechanical analysis with potential translational values. PTPRZ1-knocking down glioblastoma stem cells (GSCs) and control GSCs were used in this study. RNA were isolated using Primescript RT Master Mix (Takara). Profiling was established by applying PrimeView Affymetrix Human Gene Expression Array.
Project description:m6A RNA methylation plays an important role in regulating the self-renewal and tumorigenesis of glioblastoma stem cells. We performed m6A-seq analysis in glioblastoma stem cells with m6A levels modulated by knocking down METTL3 or METTL14 and identified m6A regulated genes in glioblastoma stem cells.
Project description:Glioblastoma stem cells (GSCs), are at the apex of its cellular hierarchy and contribute to glioblastoma progression and tumor recurrence. Gene expression profiling is useful in determining the genome-wide gene expression changes based on the experimental purpose. In order to interrogate the downstream targets of PTPRZ1, we applied gene expression profiling approach to screen the altered genes that are responsible for the functional phenotype changes. The results will provide a cue for mechanical analysis with potential translational values.
Project description:Glioblastoma progression and recurrence are suggested to be derived by glioblastoma stem-like cells (GSCs). There is limited knowledge about the expression and therapy response of LGR5 in GSCs. We have investigated the role of LGR5 in glioblastoma by knocking down LGR5 using short hairpin RNA targeting LGR5 mRNA (shLGR5) and non-target RNA (shNT) as control.
Project description:Here we have employed quantitative mass spectrometry based phosphoproteomics and proteomics to characterise the impact of knocking-down the caspase 8 gene in glioblastoma cells. This strategy enabled the identification of the pathways and processes modulated by caspase 8.
Project description:Knocking down ALKBH5 in Glioma Stem Cells resulted in an altered gene expression profile N6-methyl-adenosine (m6A) is the most prevalent internal chemical modification of mRNAs in eukaryotes. In mammals, m6A installed by m6A methyltransferases METTL3 and METTL14 is erased by two members of the AlkB family of nonheme Fe(II)/a-ketoglutarate (a-KG)-dependent dioxygenases, fat-mass and obesity associated protein (FTO) or ALKBH5. ALKBH5 affects nuclear RNA export and metabolism, gene expression and mouse fertility. To date, little is known about the biological significance of m6A in human cancer. We found that ALKBH5 is highly expressed in human glioblastoma stem cells which are resistant to conventional therapy and give rise to glioblastoma recurrence by sustaining long-term tumor growth. Global manipulation of the m6A modification by depleting ALKBH5 resulted in altered gene expression including subsets of genes enriched in "Cell Cycle", "DNA Replication, Recombination, and Repair" and "Cellular Assembly and Organization". Knockdown of ALKBH5 expression in human glioblastoma stem cells significantly reduced their self-renewal ability as a result of inhibition of cell cycle progression. This study demonstrated the important role of m6A modification in human glioblastoma development.