Project description:Protein Tyrosine Phosphatase Receptor Type N (PTPRN) plays an important role in diabetes and many cancers but its role in glioma remain poorly defined. Here, we firstly verified PTPRN expression was negatively correlated with overall survival of glioblastoma patients. Moreover, suppression of PTPRN expression reduced both U87 and U343 cell viability, suppressed proliferation, induced cell cycle arrest and inhibited glioma growth in vivo. Furthermore, KEGG and GO analysis demonstrated that PTPRN was involved in cell cycle signaling pathway, which were then confirmed by Western blot. In summary, we are the first to demonstrate that PTPRN inhibits glioma proliferation by targeting cell cycle signaling pathway. These data highlight PTPRN as a novel target for glioma treatment.
Project description:After performing an in-vivo screening with U87 glioblastoma cells transduced with a knockdown library several genes could be identified. Lin7a which was one of the candidates was further evaluated. Single knockdown of Lin7a in U87 conferred a pro-invasive phenotype in-vitro and in-vivo. Overexpression of Lin7a in the Primary glioblastoma cell line T269 reduced its invasive phenotype. To decipher the underlying pathways U87 control, U87-shLIN7a and U87-shLin7a+Lin7A (rescue cells after re-expression of Lin7A) were analyzed after in-vitro culture by a transcription profiling Array.
Project description:GPR17 over-expression inhibits glioma cell proliferation and induces apoptosis by raising ROS levels, and mechanistically inhibits the transcription of RNF2, leading to reduced histone H2A monoubiquitination. Here, To identify the genes mediating the effects of GPR17 and RNF2 on ROS level, we performed RNA-Seq of WT and U87-GPR17 cells and RNF2 ChIP-Seq of WT and U87-shGPR17 cells.
Project description:The long noncoding RNA LINC00152 shows ubiquitous expression and is often upregulated in tumor entities compared to healthy tissues. LINC00152 promotes malignant progression in the glioblastoma cell line U87. Here, LINC00152 knockdown leads to a reduction of migration and invasion of tumor cells. However, LINC00152 seems to have an opposite effect in another glioblastoma cell line A172. For this reason, the transcriptional patterns after LINC00152 knockdown in both cell lines (U87 and A172) were compared to identify the differences.
Project description:U87 cell lines were stable transfected with C19ORF63 (Human hematopoietic peptide secreted-1 - HSS1). HSS1 is a truly novel protein defining a new class of secreted factors. U87 cell line overexpressing HSS1 greatly reduced their proliferation rate compared to mock-transfected cells. Microarray analysis was used to detail gene expression underlying the anti-proliferative and anti-tumorigenic effect of HSS1 in U87 cells. Exponentially growing U87 cells at growth curve day 5 were harvested for total RNA extraction and hybridization on Affimetrix microarrays. Three groups of samples were evaluated in triplicates: U87 wild-type, U87 -pcDNA3.1 mock-transfected, U87-pcDNA-HSS1. Cells were stable transfected with pcDNA3.1 empty vector or hHSS1. hHSS1-expressing cells and control cells were at confluence 40-80% when harvested. Trypan blue analysis of the number of viable cells showed a significant anti-proliferative effect in U87 cells expressing hHSS1 as compared to the control cells.
Project description:Identify potential miR-20a regulated mRNAs and linked pathways in the setting of QK knockdown by comparing the transcriptional profiles of shQK-transduced human U87 cells together with miR-20a or a scrambled miRNA control (miR-NT)
Project description:GPR17 over-expression inhibits glioma cell proliferation and induces apoptosis by raising ROS levels, and mechanistically inhibits the transcription of RNF2, leading to reduced histone H2A monoubiquitination. Here, To identify the genes mediating the effects of GPR17 and RNF2 on ROS level, we performed RNA-Seq of WT and U87-GPR17 cells and RNF2 ChIP-Seq of WT and U87-shGPR17 cells.
Project description:This dataset examined the effect of ACTR5 knockdown in HepG2 and U87 cells. The gene expression profiling (RNA-seq) and the chromatin targeting of ACTR5 (TST-ChIP-seq) are reported.