Project description:We demonstrated that knocking down Ptbp1 can reprogram GBM cells into neuron-like cells. In order to further explore the mechanism of Ptbp1 causing this phenomenon, we performed mRNA sequencing on U251 cells infected with sh-Luci-3d, sh-Ptbp1-3d and sh-Ptbp1-7d.
Project description:Glioma is a malignant primary tumour that occurs in the central nervous system. TEA domain transcription factor (TEAD) family proteins are the Hippo pathway's ultimate effector molecules. The function of TEAD3 in gliomas is still unclear. Therefore, RNA sequencing was performed on TEAD3 knockdown U251 cells and normal U251 cells. The samples in this study included normal U251 control group and TEAD3 knockdown group. Each group contained three samples. Total RNA was extracted using Trizol reagent following the manufacturer's procedure. The total RNA quantity and purity were analysis of Bioanalyzer 2100 and RNA 6000 Nano LabChip Kit, high-quality RNA samples with RIN number > 7.0 were used to construct sequencing library. Gene Set Enrichment Analysis (GSEA) based on the sequencing results showed that knockdown of TEAD3 in the U251 cell line caused changes in several important pathways, including CTLA4 inhibitory pathway, defective pyroptosis, signaling by Hippo, regulation of TP53 activity, E2F mediated regulation of DNA replication, and FCGR3A mediated phagocytosis.
Project description:YB-1 is a cold shock domain (CSD)-containing RNA binding protein. It is involved in virtually all steps of RNA metabolism. In this study, we detected the gene expression profiles of control or YB-1 knockdown in U251 and U87 cells by performing high-throughput RNA sequencing.
Project description:Our goal is to investigate the effects of CD44 knockdown alone and in combination with Temozolomide on glioblastoma multiforme cells. To achieve this, we treated U251 cells that had been transfected with either shCtrl lentivirus or shCD44 lentivirus with either DMSO or Temozolomide.
Project description:The expression profiling of a total of 34181 mRNAs in 3 paired U251 cell line, which had been stable knockdown the expression of LINC01116.
Project description:Early passages (< 10) of frequently used GBM cell lines A172, LN18, LN229, T98G, U87-MG, U138-MG and U251-MG were characterised for genomic copy number by array CGH.
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. U87MG and hTERT/E6/E7 were retrovirally-infected with an MSCV control vector (MSCV-Control) or with a construct containing the coding region of HOXA9 (MSCV-HOXA9), resulting in U87MG-Control, U87MG-HOXA9, hTERT/E6/E7-Control and hTERT/E6/E7-HOXA9 cell lines. GBML18 and U251 cells were transfected with HOXA9 gene-specific shRNA sequences (shHOXA9) or a non-efective shRNA (shControl) in pGFP-V-RS plasmid, resulting in U251-shControl, U251-shHOXA9, GBML18-shControl and GBML18-shHOXA9 cell lines. Four experimental replicates for HOXA9 overexpression cell lines, and three for HOXA9 silencing cell lines were performed.
Project description:We generated the SRSF1 knockdown U87MG and U251 cells by infecting with shRNA virus. Then, we extracted RNAs and performed next generation sequencing. By comparing sequencing data from WT and KD samples in each cell type, we profiled the alternative splicing events and gene expression regulated by SRSF1 in GBM.
Project description:Early passages (< 10) of frequently used GBM cell lines A172, LN18, LN229, T98G, U87-MG, U138-MG and U251-MG were characterised for global DNA methylation patterns.
