The long noncoding RNA NORAD promotes the growth of gastric cancer cells by sponging miR-608.

Dysfunction of long non-coding RNAs (lncRNAs) has been suggested to play pivotal roles in the initiation and progression of human cancers. The noncoding RNA activated by DNA damage (NORAD) is a recently identified, highly conserved lncRNA that is essential for the mitotic cell division. Recent studies demonstrated the potential oncogenic function of NORAD in bladder cancer and colon cancer, however, the role and clinical value of NORAD have not been illustrated in gastric cancer. Here, we found that NORAD was highly expressed in gastric cancer tissues and cell lines. Overexpression of NORAD was significantly correlated with the worse prognosis of the gastric cancer patients. Down-regulation of NORAD suppressed the proliferation and migration of gastric cancer cells. Mechanistically, NORAD acted as a competitive endogenous RNA (ceRNA), which sponged miR-608 and suppressed the expression of miR-608 in gastric cancer cells. Further experiments demonstrated that miR-608 targeted the forkhead box O6 (FOXO6) and negatively regulated the expression of FOXO6. Consistent with the inhibitory effect of NORAD on miR-608, overexpression of NORAD enhanced the level of FOXO6 in gastric cancer cells. Overexpression of FOXO6 attenuated the inhibitory effect of miR-608 on the gastric cancer cell growth. Collectively, our results demonstrated that NORAD promoted the growth of gastric cancer cells via modulating the miR-608/FOXO6 pathway.