Long non-coding RNA DLEUl promotes cell proliferation of glioblastoma multiforme

Abstract

Glioblastoma multiforme (GBM) is the most common malignant tumor with high morbidity and mortality. This study investigated the role of long non-coding RNAs (lncRNAs) in glioblastomagenesis progression. Using the G S E 2 2 2 3 and G S E 5 9 6 1 2 datasets, and R N A sequencing data of GBM from The Cancer Genome Atlas, differentially expressed (DE) genes including DE messenger RNAs (DEmRNAs) and DElncRNAs between GBM and normal controls were identi¬ fied. Based on the competing endogenous RNA hypothesis, DElncRNA-micro RNA (miRNA)-DEmRNA interactions were obtained by target gene prediction. Gene Ontology (GO) and Kyoto encyclopedia of Gene and Genomes pathway analysis of DEmRNAs in the DElncRNA-miRNA-DEmRNA network was performed. Expression and function analyses of DElncRNAs were performed by reverse transcription-polymerase chain reaction (RT-PCR) and an established viability assay, respectively. In total, 712 DE genes were identified. Significant upregulation of lncRNA deleted in lymphocytic leukemia 1 (DLEU1) was revealed in GBM and a number of other types of cancer. D L E U 1 interacted with 315 miRNAs and 105 DEmRNAs. The DEmRNAs were mainly enriched in tumorigenesis-associated GO terms (angiogenesis, positive regulation of cell proliferation, positive regulation of fibroblast apoptotic processes and regulation of neutrophil migration) and pathways (Hippo signaling pathway, cancer pathways, and Wnt signaling pathway). Correlation analysis revealed that mRNA TNF receptor associated factor 4 (T R A F 4) was associated with D L E U 1 expression. R T - P C R demonstrated that the expression levels of DLEU1 and TRAF4 were increased in GBM tissues. Small interfering RNA demonstrated that silencing DLEU1 downregulated TRAF4. The viability of GBM cells was significantly decreased following RNA interference with DLEU1 and TRAF4 production. The results demonstrate that DLEU1 and TRAF4 is highly expressed in GBM tissues and promotes proliferation of GBM cells. It may act as a competing endogenous RNA and influence tumorigenesis of GBM.