Abstract
Objective: To investigate the effects of long non-coding RNA HULC on downstream related targets regulating the migration and invasion of hepatoma cells and theirs mechanism of action. Methods: The expression of highly upregulated in liver cancer (HULC) in hepatocellular carcinoma, and adjacent normal liver tissues and different hepatocellular carcinoma cells were detected by qPCR. The correlation between clinicopathological data of HULC and liver cancer patients were analyzed. Dual-luciferase reporter gene detected the interaction between HULC and miR-186. CCK-8 assay was used to detect the effect of HULC on proliferation of hepatocellular carcinoma cells. The change in hepatocellular carcinoma cell invasions ability after HULC inhibition was detected by transwell invasion assay and migration ability after inhibition of HULC was assessed by scratch assay. Differences between groups were compared using one-way ANOVA. P < 0.05 was considered statistically significant. Results: Compared with adjacent normal liver tissue, the expression of HULC in hepatocellular carcinoma was significantly higher [(1.79 ± 0.25) vs. (0.23 ± 0.05), P < 0.05]. The expression level of HULC was highest in hepatocellular carcinoma HepG3 cells. HULC specifically banded to the 3'UTR of miR-186 and regulated the expressional activity of miR-186. After inhibiting the expression of HULC, the proliferation of hepatocellular carcinoma cells was 72 h (0.35 ± 0.09) vs. (0.82 ± 0.16), P < 0.05; 96 h (0.42 ± 0.08) vs.(1.28 ± 0.19), P < 0.05), and the ability of migration and invasion was relatively decreased in 24 h (11.2% ± 1.6%) vs. (23.5% ± 3.6%), P < 0.05; 48 h (18.6% ± 3.0%) vs. (38.6% ± 5.6%), P < 0.05; 72 h (43.6% ± 5.3% ) vs. (69.6% ± 7.6%), P < 0.05]. After inhibiting the expression of HULC, the tumor volume and body weight of tumor-bearing mice were significantly reduced [volume (2.89 ± 0.29) cm(3) vs. (0.89 ± 0.18) cm(3), P < 0.05, body weight (3.18 ± 0.41) g vs. (0.45 ± 0.09) g, P < 0.05]. Conclusion: HULC plays an important role in the occurrence and development of hepatocellular carcinoma and can influence the biological behavior of hepatoma cells by regulating the expression of downstream-related targets.