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: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:Genome wide DNA methylation profiling of control and mTORC2-suppressed glioblastoma cells (U87-EGFRvIII cells). The Illumina Infinium HumanMethylation EPIC BeadChip Array was used to obtain DNA methylation profiles with 865,918 probes in glioblastoma cell line samples. Samples included 2 control U87-MG cells without mTORC2 suppresion, and mTORC2-knockdown U87-MG cells with lentivirus-mediated suppression of mTORC2.
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:Purpose:Next-generation sequencing has revolutionized sytems-level celluar pathway analysis. The goals of this study are to compare the U87 cell xenograft GBM mice (U87 cell line) to TWIST1 knock out U87 cell xenograft GBM mice (TWIST1 knock out U87 cell line) using their transcriptomes
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:The objective of the study was to examine the gene expression changes in glioma cell line U87 and U251 with LAMP2A knockdown. There were 15 samples in total- U87-1, U87-2, U87-3, U87-1812-1, U87-1812-2, U87-1812-3, U251-1, U251-2, U251-3, U251-1812-1, U251-1812-2, U251-1812-3, U251-1813-1, U251-1813-2, and U251-1813-3. U87-1 to U87-3 and U251--1 to U251-3 were used as the control groups (CON). U87-1812-1 to U871812-3, U251-1812-1 to U251-1812-3, and U251-1813-1 to U251-1813-3 were used as the experimental groups (shLAMP2A-1 and shLAMP2A-2). The total RNA of each sample was extracted from the stable transfected glioma cells by using TRIzol reagent. Then the RNA samples were processed for high throughput transcriptome sequencing on Illumina HiSeq 3000 platform. There were two types of libraries: the circRNA, mRNA, and lncRNA were all constructed by removing rRNA (one library, three types of RNA were analyzed together), and the insert fragment was about 300bp; the small RNA was constructed and analyzed separately, mainly microRNA of about 22bp. Results: among 60612 cleaned mRNAs, 781 were differentially expressed in U87-1812 group compared with U87 group, 146 were differentially expressed in U251-1812 group compared with U251 group, 43 were differentially expressed in U251-1813 group compared with U251 group (padj ≤ 0.05 and expression change ≥2 fold). The differential expressed genes distributed in all chromosomes. Functional annotation with GO and KEGG enrichment revealed the top functional groups including inflammation, DNA replication, cell adhesion, TNF, IL17, and axon guidance signaling pathways.