RNA sequencing analysis of human glioblastoma cell line U87MG treated with LMO2 overexpression.
Ontology highlight
ABSTRACT: To understand the changes in the expression of genes in U87MG cells due to LMO2, we analyzed the transcriptome of U87MG cells overexpressing LMO2. As a result, we identify differentially expressed genes patterns so that the signaling mechanism regulated by LMO2 in GBM and changes in cells were observed. These RNA sequencing analysis results enable an understanding of the signaling mechanism by LMO2 in GBM.
Project description:To understand the changes in the expression of genes in U87MG cells due to ID Family, we analyzed the transcriptome of U87MG cells overexpressing ID Family. As a result, we identify differentially expressed genes patterns so that the signaling mechanism regulated by ID Family in GBM and changes in cells were observed. These mRNA expression profiling analysis results enable an understanding of the signaling mechanism by ID Family in GBM.
Project description:To explore factors contributing to radioresistance in GBM, we established GBM radioresistant cell line using U87MG human GBM cells.
Project description:Glioblastoma (GBM) is the most lethal primary brain cancer that lacks effective molecular targeted therapies. PI3K/AKT/mTOR signaling pathway is activated in 90% of all Glioblastoma Multiforme (GBM) tumors. To gain insight into the impact of the PI3K Pathway on GBM metabolism, we treated U87MG GBM cells with 50nM NVP-BEZ235 (PI3K and mTOR a dual inhibitor) for four days and identified differentially expressed genes with RNA-seq analysis.
Project description:This study investigated the biological function of ABCB7 in U87MG glioblastoma cell line. Many ABC transporters are known contributions to drug resistance and various biological process. However, mitochondrial ABC transporters aren’t known mechanism to control biological process. We identified the potential roles of ATP-binding cassette (ABC) transporter subfamily member 7 (ABCB7), one of the mitochondrial ABC transporters. ABCB7 activates signaling pathway of hypoxia-inducible factor 1 alpha (HIF1α) by hypoxia independent regulation. This signaling pathway regulates the death inhibitory genes and survival related genes. Also, ABCB7 downregulates cell cycle related genes. Our results provide that ABCB7 is essential for the survival of malignant brain tumors.
Project description:This study investigated the biological function of CD133 by ectopic expression of CD133 in U87MG cell line. Although CD133 is widely used as a cancer stem cell marker, there are a few studies that examined its own biological functions. While a number of loss-of-function studies about CD133 have shown that CD133 have effects on cancer progression, there are few gain-of-function studies about functions of CD133. Thus, we identified the potential function of CD133 by its overexpression in U87MG glioblastoma cell line. Though there were no significant changes in cell growth and sphere forming ability, elevated IL-1β and its downstream chemokines (CCL3, CXCL3, CXCL5) may function as chemoattractants which affect recruitment of Ly6G+ neutrophils surrounding necrotic regions in vivo and migration of neutrophil-like dHL-60 cells. Taken together, this results imply that CD133 can regulate IL-1β signaling, and promotes the environmental change.
Project description:EGFRvIII is the most common deletion mutant of EGFR in human cancer and its levels are highly correlated with poor prognosis in GBM. The deletion of exons 2-7 removes most of the extracellular ligand binding domain, so it is unable to bind EGF or other EGFR-binding ligands. Nevertheless, the mutant receptor is constitutively phosphorylated, and is capable of activating downstream signaling pathways at a low level. To comprehensively identify the downstream signaling consequences of the EGFRvIII, we incorporated phosphoproteomic, transcription profiling and DNase-Seq data from U87MG glioblastoma cells expressing titrated levels of this mutant receptor. Total RNA were extracted from U87MG cells engineered to expressed different levels of EGFRvIII: medium (U87M; 1.5 million copies of EGFRvIII receptor per cell), high (U87H; 2 million copies per cell), super-high (U87SH; 2.5 million copies per cell), and kinase-dead EGFRvIII (U87DK; 2 million copies of kinase dead EGFRvIII per cell). RNA was hybridized to Affymetrix microarrays.
Project description:EGFRvIII is the most common deletion mutant of EGFR in human cancer and its levels are highly correlated with poor prognosis in GBM. The deletion of exons 2-7 removes most of the extracellular ligand binding domain, so it is unable to bind EGF or other EGFR-binding ligands. Nevertheless, the mutant receptor is constitutively phosphorylated, and is capable of activating downstream signaling pathways at a low level. To comprehensively identify the downstream signaling consequences of the EGFRvIII, we incorporated phosphoproteomic, transcription profiling and DNase-Seq data from U87MG glioblastoma cells expressing titrated levels of this mutant receptor.
Project description:Assess gene expression patterns upon HOXA9 ectopic expression in U87MG GBM cell line and hTERT/E6/E7 immortalized human astrocytes, and HOXA9 silencing in U251 and GBML18 GBM cell lines.