Abstract
OBJECTIVES: Prostate cancer (PCA) is the deadliest urological disease affecting men worldwide. Long noncoding RNA activated by DNA damage (NORAD) levels are increased in many cancer types, and induce cancer cell progression. However, little is known about the biological functions of NORAD in PCA. METHODS: In this work, the roles of NORAD in cell proliferation, migration, and apoptosis were examined by Cell Counting Kit-8, scratch wound, and annexin V-fluorescein isothiocyanate/propidium iodide staining assays, respectively, in PCA cell lines. Knockdown of NORAD was achieved by small interfering (si)RNA in PCA cell lines, and quantitative real-time PCR was used to detect the expression of NORAD. RESULTS: Cell proliferation and migration rates were significantly lower in the siNORAD group than in the wild-type group, while the apoptosis level was significantly higher in the siNORAD group compared with the wild-type group. CONCLUSIONS: These results suggest that NORAD promotes the proliferation and migration of PCA cells and inhibits their apoptosis.