MiR-424 suppressed viability and invasion by targeting to the DCLK1 in neuroblastoma.

Abstract

Neuroblastoma is the most frequent tumor of sympathetic nervous system in infants. MiRNAs acted as oncogenes or tumor suppressors in the process of tumor development. We aim at exploring the functions of miRNA in neuroblastoma. Cell viability and invasion were evaluated by Cell Counting Kit-8 (CCK-8) and transwell assays. Western blot was utilized to assess the protein expression associated with epithelial-mesenchymal transition (EMT) markers. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to calculate the mRNA levels of miRNA and gene. MiR-424 was downregulated while doublecortin like kinase 1 (DCLK1) was upregulated in neuroblastoma tissues and cells compared to adjacent non-tumor and normal spongiocyte cells. MiR-424 suppressed cell viability, invasion, and EMT by targeting DCLK1. MiR-424 regulated the expression of DCLK1 by directly binding to the 3'-untranslated region (UTR) of DCLK1 mRNA in SK-N-SH and Be2C cells. DCLK1 reversed partial functions of miR-424 in neuroblastoma. MiR-424 suppressed cell viability, invasion, and EMT by directly targeting the 3'-UTR of DCLK1 mRNA. The newly identified miR-424/DCLK1 axis provides novel insights into the pathogenesis of neuroblastoma.