DGCR5 suppresses the EMT of pediatric primary glioblastoma multiforme cell and serves as a prognostic biomarker.

Abstract

Pediatric primary glioblastoma multiforme (GBM) is a common brain tumor among childhood. Nevertheless, the underlying mechanism of glioblastoma progresses remains to be illuminated. The current study explores the potential functions of long noncoding RNA (lncRNA) DGCR5 in the aggressiveness of GBM. The expression of DGCR5 was evaluated by quantitative real-time PCR (qRT-PCR). Immunoblotting was carried out to assess the protein expressions of N-cadherin and E-cadherin. Cell Counting Kit-8 (CCK-8), wound healing, transwell assay, and flow cytometry were applied to explore the roles of DGCR5 in glioblastoma cell malignant biological behaviors. LncRNA DGCR5 was down expressed in glioblastoma. Transfection of DGCR5 markedly repressed cell viability and colony formation ability of U87 and U251 cells. Additional, DGCR5 overexpression caused cell cycle arrest and increased cell apoptosis. Moreover, upregulation of DGCR5 suppressed the growth and promoted cell apoptosis of U87 cell in vivo. Finally, overexpression of DGCR5 impaired the migration, invasiveness, and reversed epithelial-to-mesenchymal transition (EMT) process of glioblastoma cell. LncRNA DGCR5 inhibited the proliferation, aggressiveness phenotypes, and EMT of glioblastoma cell.