Long Non Coding RNA SNHG16 Facilitates Proliferation, Migration, Invasion and Autophagy of Neuroblastoma Cells via Sponging miR-542-3p and Upregulating ATG5 Expression

BACKGROUND: Neuroblastoma (NB) is a heterogeneous pediatric malignant tumor with many biological and clinical characteristics. Long non-coding RNA small nucleolar RNA host gene 16 (SNHG16) plays vital role in the development of NB. However, the potential mechanism of SNHG16 in the progression of NB is rarely reported. METHODS: The expression levels of SNHG16, miR-542-3p and autophagy-related gene 5 (ATG5) were measured with quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, migration and invasion of NB cells were determined using 3-(4, 5-dimethylthiazol-2-YI)-2, 5-diphenyltetrazolium bromide (MTT) or transwell assay. Protein levels of ATG5, microtubule-associated protein A1/1B-light chain3 (LC3-I/II) and p62 were detected by Western blot analysis. The interaction between miR-542-3p and SNHG16 or ATG5 was predicted by starBase and confirmed by dual luciferase reporter assay. Xenograft mice models were constructed to confirm the role of SNHG16 in vivo. RESULTS: SNHG16 was upregulated in NB tissues and cells and associated with clinical stage and poor prognosis of NB. Knockdown of SNHG16 impeded proliferation, migration, invasion and autophagy of NB cells in vitro, and suppressed tumor growth in vivo. Interestingly, SNHG16 mediated ATG5 expression through sponging miR-542-3p in NB cells. Moreover, miR-542-3p downregulation reversed the inhibitory effects of SNHG16 silencing on proliferation, migration, invasion and autophagy of NB cells. Besides, ATG5 overturned the regulatory effects on proliferation, migration, invasion and autophagy of NB cells induced by SNHG16 or miR-542-3p knockdown. CONCLUSION: SNHG16 facilitated proliferation, migration, invasion and autophagy of NB cells via sponging miR-542-3p and upregulating ATG5 expression in NB.