Abstract
Non-coding RNA has been reported to be crucial regulator for cancer progression. This work was aimed to investigate the roles and associated mechanisms of non-coding RNA activated by DNA damage (NORAD) in hepatocellular carcinoma (HCC) progression. In this work, we explored the expression of NORAD, microRNA-144-3p (miR-144-3p), and septin 2 (SEPT2) in HCC tissues and cells. Effects of knockdown of ectopic of NORAD on HCC cell proliferation, colony formation, and apoptosis were explored. Rescue experiments were conducted to explore whether NORAD regulates HCC cell behaviors via the miR-144-3p/SEPT2 axis. Moreover, the effect of NORAD on HCC tumor progression in vivo was analyzed. We showed NORAD expression was elevated in both HCC tissues and cells. NORAD knockdown inhibits HCC cell growth but promotes apoptosis, while the overexpression of NORAD has opposite effects. Besides that, we found knockdown of NPRAD inhibits tumor growth. Moreover, we showed miR-144-3p expression was inversely correlated with NORAD and SEPT2, while NORAD and SEPT2 was positively correlated in HCC tissues. Functional assays showed NORAD functions as ceRNA through binding with miR-144-3p to regulate SEPT2 expression in HCC. Collectively, we showed NORAD serves as an oncogenic lncRNA to promote HCC progression via the miR-144-3p/SEPT2 axis.