LncRNA SNHG16 promotes epithelial- mesenchymal transition via down-regulation of DKK3 in gastric cancer.

Recent studies have shown that long noncoding RNAs (lncRNAs) have profound impacts on cancer development. In our previous study, we have confirmed that lncRNA small nucleolar RNA host gene 16 (SNHG16) is associated with poor prognosis and malignant phenotype of gastric cancer (GC). However, the biological function of lncRNA SNHG16 is still unclear. Here, we aimed to investigate the mechanisms underlying the roles of SNHG16 in GC. In this work, SNHG16 knockdown could inhibit epithelial-mesenchymal transition (EMT) and invasion of GC cells. Moreover, our results revealed that SNHG16 could promote EMT via down-regulation of Dickkopf WNT signaling pathway inhibitor 3 (DKK3) in GC cells. In addition, SNHG16 was found to be upregulated whereas DKK3 was downregulated in tumor tissues compared with adjacent normal tissues. It showed that the expressions of SNHG16 and DKK3 were negatively correlated in clinical GC tissues.All these results suggested that SNHG16 promotes GC progression via regulation of DKK3 directly or indirectly. SNHG16 might be used as a putative biomarker for metastatic prediction in GC patients.