OBJECTIVE: Recently, the role of long noncoding RNAs (lncRNAs) is vital in tumor progression. Our study aims to identify the role of SNHG16 in the metastasis of pancreatic carcinoma. PATIENTS AND METHODS: Real-Time quantitative Polymerase Chain Reaction (RT-qPCR) was used to measure SNHG16 expression in 56 pancreatic carcinoma patients' tissues. Function assays, including wound healing assay, and transwell assay, were conducted to detect the effect of SNHG16 on the metastasis of pancreatic carcinoma. Besides, the luciferase assay was performed to explore the underlying mechanism. RESULTS: The expression level of SNHG16 was upregulated in pancreatic carcinoma samples compared with adjacent tissues. Moreover, cell migration and cell invasion were repressed via the knockdown of SNHG16, while cell migration and cell invasion were promoted via the overexpression of SNHG16. Moreover, the expression of miR-200a-3p was upregulated via knockdown of SNHG16 while the expression of miR-200a-3p was downregulated via the upregulation of SNHG16 in vitro. Furthermore, it was discovered that SNHG16 acted as a competing endogenous RNA via sponging miR-200a-3p in pancreatic carcinoma. CONCLUSIONS: Our study suggests that SNHG16 acts as an oncogene in pancreatic carcinoma and promotes cell metastasis via sponging miR-200a-3p, which might be a novel therapeutic strategy in pancreatic carcinoma.
OBJECTIVE: Recently, the role of long noncoding RNAs (lncRNAs) is vital in tumor progression. Our study aims to identify the role of SNHG16 in the metastasis of pancreatic carcinoma. PATIENTS AND METHODS: Real-Time quantitative Polymerase Chain Reaction (RT-qPCR) was used to measure SNHG16 expression in 56 pancreatic carcinomapatients' tissues. Function assays, including wound healing assay, and transwell assay, were conducted to detect the effect of SNHG16 on the metastasis of pancreatic carcinoma. Besides, the luciferase assay was performed to explore the underlying mechanism. RESULTS: The expression level of SNHG16 was upregulated in pancreatic carcinoma samples compared with adjacent tissues. Moreover, cell migration and cell invasion were repressed via the knockdown of SNHG16, while cell migration and cell invasion were promoted via the overexpression of SNHG16. Moreover, the expression of miR-200a-3p was upregulated via knockdown of SNHG16 while the expression of miR-200a-3p was downregulated via the upregulation of SNHG16 in vitro. Furthermore, it was discovered that SNHG16 acted as a competing endogenous RNA via sponging miR-200a-3p in pancreatic carcinoma. CONCLUSIONS: Our study suggests that SNHG16 acts as an oncogene in pancreatic carcinoma and promotes cell metastasis via sponging miR-200a-3p, which might be a novel therapeutic strategy in pancreatic carcinoma.