Expression of Long Non-Coding RNA (lncRNA) Small Nucleolar RNA Host Gene 1 (SNHG1) Exacerbates Hepatocellular Carcinoma Through Suppressing miR-195
Hui Zhang, Dong Zhou, Mingang Ying, Minyong Chen, Peng Chen, Zhaoshuo Chen, Fan Zhang
Department of Abdominal Surgery, Fujian Provincial Cancer Hospital, Fujian Medical University Teaching Hospital, Fuzhou, Fujian, China (mainland)
Med Sci Monit 2016; 22:4820-4829
Aberrant expression of lncRNA has been suggested to have an association with tumorigenesis. Our study was designed to reveal the underlying connection between lncRNA SNHG1 and hepatocellular carcinoma (HCC) pathogenesis.
MATERIAL AND METHODS: A total of 122 pairs of HCC tissues (case group) and matched adjacent non-tumor liver tissues (control group) were collected for this study. RT-PCR and in situ hybridization were conducted to investigate differences in lncRNA SNHG1 expression between the case and control group. The expression levels of lncRNA SNHG1 and miR-195 in HepG2 cells transfected with SNHG1-mimic and SNHG1-inhibitor were measured by RT-PCR. The proliferation, invasion, and migration status of HepG2 cells after transfection were assessed through MTT assay, wound healing assay, and Transwell assay, respectively. Whether miR-195 is a direct downstream target of lncRNA SNHG1 was verified by both bioinformatics target gene prediction and dual-luciferase report assay.
RESULTS: The expression level of lncRNA SNHG1 was remarkably upregulated in HCC tissues and cell lines compared with normal tissues and cell lines. High expression of lncRNA SNHG1 contributed to the downregulation of miR-195 in HepG2 cells. Also, lncRNA SNHG1 exacerbated HCC cell proliferation, invasion, and migration in vitro through the inhibition of miR-195. This suggests that miR-195 is a direct downstream target of lncRNA SNHG1.
CONCLUSIONS: lncRNA SNHG1 may contribute to the aggravation of HCC through the inhibition of miR-195.
Keywords: Cell Line, Tumor, Carcinoma, Hepatocellular - pathology, Cell Movement - genetics, Cell Proliferation - genetics, Cell Transformation, Neoplastic - genetics, Down-Regulation, Gene Expression Regulation, Neoplastic, Hep G2 cells, Liver Neoplasms - genetics, MicroRNAs - metabolism, RNA, Long Noncoding - metabolism, RNA, Small Nucleolar - genetics, Transfection, Up-Regulation