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Endogenous bornavirus-like nucleoprotein elements ( EBLN  s ) have been discovered in the genomes of various animals including humans, whose functions have been seldom studied. To explore the biological functions of human  EBLNs , we constructed a lentiviral vector expressing a short-hairpin RNA against human  EBLN1 , which successfully inhibited  EBLN1  expression by above 80% in infected human oligodendroglia cells (OL cells). We found that  EBLN1  silencing suppressed cell proliferation, induced G2/M phase arrest, and promoted apoptosis in OL cells. Gene expression profiling demonstrated that 1067 genes were up-regulated, and 2004 were down-regulated after  EBLN1  silencing. The top 10 most upregulated genes were  PI3 ,  RND3 ,  BLZF1 ,  SOD2 ,  EPGN ,  SBSN ,  INSIG1 ,  OSMR ,  CREB3L2 , and  MSMO1 , and the top 10 most-downregulated genes were  KRTAP2-4 ,  FLRT2 ,  DIDO1 ,  FAT4 ,  ESCO2 ,  ZNF804A ,  SUV420H1 ,  ZC3H4 ,  YAE1D1 , and  NCOA5 . Pathway analysis revealed that these differentially expressed genes were mainly involved in pathways related to the cell cycle, the mitogen-activated protein kinase pathway, p53 signaling, and apoptosis. The gene expression profiles were validated by using quantitative reverse transcription polymerase chain reaction (RT-PCR) for detecting these 20 most-changed genes. Three genes closely related to glioma,  RND3 ,  OSMR , and  CREB3L2 , were significantly upregulated and might be the key factors in  EBLN1  regulating the proliferation and apoptosis of OL cells. This study provides evidence that  EBLN1  plays a key role in regulating cell life and death, thereby opening several avenues of investigation regarding  EBLN1  in the future.

Knock-Down of Endogenous Bornavirus-Like Nucleoprotein 1 Inhibits Cell Growth and Induces Apoptosis in Human Oligodendroglia Cells