The expression of long noncoding RNA small nucleolar RNA host gene 12 in hepatocellular carcinoma and its mechanism

Abstract

Objective To investigate the expression level of small nucleolar RNA host gene 12 (SNHG12) in hepatocellular carcinoma (HCC) tissue and its mechanism on the growth and invasion of hepatoma cells. Methods We determined the expression level of SNHG12 in 50 HCC patients collected from Zhongnan Hospital of Wuhan University with real-time reverse transcriptase-polymerase chain reaction (RT-qPCR) and then studied its clinical significance. SiRNA interference was used to knock down the SNHG12 level in vitro. In addition, Transwell assay and methyl thiazol tetrazolium (MTT) assay were uesd to observe the changes in growth and invasion of hepatoma cells. Western blotting was used to detecte the change of key molecules in transforming growth factor-β (TGF-β)/Smad pathway after SNHG12 was silenced. Results SNHG12 was upregulated in HCC tissues (2.943±0.881) as compared with adjacent tissues (1.613±0.533, P=0.007). HCC patients whose tumor diameter >5 cm had a higher SNHG12 level (4.024±0.281) than those with tumor diameter ≤5 cm (2.591±0.394, P=0.002). HCC patients with a higher Edmonson-Steiner grade had a higher SNHG12 level (P=0.001). SNHG12 was closely associated with tumor diameter (P=0.000), Edmonson-Steiner grade (P=0.003) and metastasis (P=0.031). Furthermore, Kaplan-Meier and Log-rank test analyses suggested that HCC patients with high SNHG12 expression had shorter overall survival (P=0.009) and higher recurrence rate than those with low expression of SNHG12 (P=0.001). SNHG12 promoted hepatoma cell growth and invasion by regulating the TGF-β/Smad pathway. Conclusion These findings indicate that SNHG12 is a critical molecule for HCC progression and is potentially a new effective target for HCC therapy. Key words: Carcinoma, hepatocellular; Small nucleolar RNA host gene 12; Growth; Invasion