Long noncoding RNA SNHG16 acts as an oncogene in Wilms' tumor through sponging miR-200a-3p.

OBJECTIVE

Recently, the role of long noncoding RNA (lncRNAs) in tumor progression has attracted much attention. The aim of this study was to investigate the role of lncRNA SNHG16 in the development of Wilms' tumor, and to explore the underlying mechanism.

PATIENTS AND METHODS

Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect SNHG16 expression in Wilms' tumor patients' tissues. Function assays, including wound healing assay, and transwell assay, were conducted to detect the changes of biological behaviors in Wilms' tumor cells due to gain or loss of SNHG16. Besides, the luciferase reporter gene assay was performed to explore the underlying mechanism.

RESULTS

The expression level of SNHG16 was significantly up-regulated in Wilms' tumor tissues when compared with adjacent tissues. Cell migration and invasion abilities were significantly repressed via down-regulation of SNHG16. However, opposite results were obtained after up-regulation of SNHG16 in vitro. After the down-regulation of SNHG16, the expression of miR-200a-3p increased significantly. However, the expression of miR-200a-3p was remarkably reduced via up-regulation of SNHG16 in vitro. Furthermore, SNHG16 acted as a competing endogenous RNA via sponging miR-200a-3p in Wilms' tumor.

CONCLUSIONS

SNHG16 induced the metastasis of Wilms' tumor via sponging miR-200a-3p. Our findings might provide a new prospect for the diagnosis and therapy of Wilms' tumor.