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:Differential transcriptome analysis between control cells (U87MG), TMZ-resistant cells with continuous TMZ treatment (U87MG R50) and TMZ-resistant cells with interrupted treatment (U87MG OFF R50).
Project description:Next-generation sequencing (NGS) has significantly advanced the elucidation of developmental signaling mechanisms that are important for U87MG cells under differente treatment. We report here the application of RNA-sequencing technology for transcriptome profile of U87MG cells treated with CAR neutrophils, nanodrugs, and CAR neutrophils loaded nanodrugs. Six U87MG samples were performed in IIIumina HiSeq2500. The resulting sequence reads were mapped to human genome (hg19) using HISAT, and the RefSeq transcript levels (RPKMs) were quantified using the python script rpkmforgenes.py. Our RNA-seq data analyzed different cellular signal pathways under treatment. This study shows a detailed analysis of U87MG transcriptomes generated by RNA-seq technology, providing insight into the mechanisms underlying CAR neutrophils lysis the tumor cells.
Project description:EGFRvA is a novel and widely-expressed EGFR isoform, whose upregulation is positively related to glioma grades. Intriguingly, it is the upregulation of EGFRvA but not EGFR that significantly correlates with a poor prognosis in glioma patients. Cancer cells expressing EGFRvA (relative to EGFR) display a higher invasive capacity and a lower sensitivity to EGFR tyrosine kinase inhibitors (TKIs). To investigate the significant differently expressed genes between U87MG EGFRvA cells and U87MG EGFR cells,microarray experiments were conducted.
Project description:We established tumorspheres from human glioblastoma U87MG cells by single cell-derived tumorsphere formation. Among these tumorspheres, P4E8 clone showed cancer stem cell like properties such as self-renewal capacity, expression of cancer stem cell markers, resistance to anti-cancer agents and in vivo tumorigenicity. To find novel therapeutic target molecules, we performed differential gene expression analysis between U87MG and P4E8 cells.
Project description:EGFRvA is a novel and widely-expressed EGFR isoform, whose upregulation is positively related to glioma grades. Intriguingly, it is the upregulation of EGFRvA but not EGFR that significantly correlates with a poor prognosis in glioma patients. Cancer cells expressing EGFRvA (relative to EGFR) display a higher invasive capacity and a lower sensitivity to EGFR tyrosine kinase inhibitors (TKIs). To investigate the significant differently expressed genes between U87MG EGFRvA cells and U87MG EGFR cellsM-oM-<M-^Lmicroarray experiments were conducted. Gene-expression profiling was performed on the CapitalBio 35k human Genome Array microchips (Beijing, China).
Project description:U87MG is a glioblastoma cell line that shows substantial heterogeneity despite long-term passaging. We used microarrays to identify variations in gene expression that are associated with phenotypic differences among subclones derived from U87MG.
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: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.