Abstract
BACKGROUND: Small nucleolar RNA host gene 17 (SNHG17), a novel cancer-related long noncoding RNA (lncRNA), was reported to be responsible for processing and developing in several cancers. Nonetheless, the clinical significance and biological function of SNHG17 in human breast cancer (BC) remain rarely known. MATERIALS AND METHODS: 58 pairs of BC tissues and adjacent non-cancerous tissues were harvested to measure SNHG17 expression levels. SNHG17 was knockdown to study its biological behavior in BC cells. The microRNAs (miRNAs) that can bind to SNHG17 were predicated using Starbase2.0 and were tested using luciferase reporter activity and RIP assays. A xenograft model was established to investigate the impact of SNHG17 in tumor growth in vivo. RESULTS: An increased SNHG17 was observed in BC samples and cell lines compared with corresponding control. Increased SNHG17 was closely associated with poor prognosis.SNHG17 depletion suppressed cell proliferation, migration and invasion in vitro, as well as inhibited tumor growth in xenograft tumor models. Mechanistically, SNHG17 could function as an endogenous sponge of miR-124-3p in BC cells. Moreover, the repression of cell proliferation, migration and invasion induced by SNHG17 knockdown would reversed by miR-124-3p inhibitor. CONCLUSION: The present study demonstrated that the lncRNASNHG17 could regulate the progression of BC by sponging miR-124-3p.