The effect of TRIP13 on glioma cell function and signaling pathways

To gain insight into the molecular mechanisms underlying TRIP13-mediated oncogenic activity in GBM, we performed RNA-seq on spheres derived from U87MG-shTRIP13 and control cells .This analysis identified 1094 genes whose expression was markedly reduced by TRIP13 knockdown in U87MG-derived spheres (fold change >2, p < 0.05; Supplementary ). These downregulated genes were highly overrepresented in gene ontologies (GO) that are associated with growth factor activity, angiogenesis and chemotaxis. Gene set enrichment analysis (GSEA) showed that genes related to phosphatidylinositol 3-kinase (PI3K/AKT) pathway and genes involved in pluripotency of stem cells were significantly altered in TRIP13 knockdown GBM cells . KEGG pathway analysis revealed that the altered genes were enriched to PI3K–AKT signaling, JAK-STAT signaling and cytokine-cytokine receptor interaction. We conclude that RNA-seq based transcriptome characterization would expedite cancer signaling pathway analyses. Overall design: Differential mRNA expression analysis of two groups