Long non-coding RNA SNHG7 promotes neuroblastoma progression through sponging miR-323a-5p and miR-342-5p

Abstract

Dysregulation of long non-coding RNAs (lncRNAs) has been known to be relevant to the progression of human cancers, including neuroblastoma (NB). Small nucleolar RNA host gene 7 (SNHG7) has been identified as an oncogene in a series of human cancers. The purpose of the present study was to investigate the function and underlying mechanism of SNHG7 in NB progression. qRT-PCR was used to determine the levels of SNHG7, cyclin D1 (CCND1), miR-323a-5p and miR-342-5p. Cell migration and invasion abilities were detected by transwell assays. Glucose consumption and lactate production were assessed using the corresponding assay kits. The targeted interaction between SNHG7 and miR-323a-5p or miR-342-5p was verified by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Xenograft tumor assays were performed to observe the effect of SNHG7 silencing on tumor growth in vivo. We found that SNHG7 was upregulated in NB tissues and cell lines, and high SNHG7 level was relevant to poor prognosis of NB patients. SNHG7 silencing resulted in the repression of NB cell migration, invasion and glycolysis. SNHG7 directly targeted miR-323a-5p and miR-342-5p and negatively modulated their expression in NB cells. The overexpression of miR-323a-5p or miR-342-5p weakened NB cell migration, invasion and glycolysis. Moreover, miR-323a-5p or miR-342-5p mediated the suppressive effect of SNHG7 silencing on NB cell progression. CCND1 was a direct target of miR-323a-5p and miR-342-5p. Additionally, SNHG7 knockdown repressed tumor growth in vivo. In conclusion, our study suggested that SNHG7 silencing hindered NB progression at least partly though sponging miR-323a-5p and miR-342-5p, illuminating its potential value as a therapeutic target.