Abstract
Hepatocellular carcinoma (HCC) is one of the most famous fatal malignancies in the world. LncRNA SNHG1 has been shown to play roles in the development and progression of various tumors, including HCC. The present study aims to investigate the deeper molecular mechanisms of SNHG1 in HCC. The expression levels of SNHG1 and miR-377-3p were detected by qRT-PCR in HCC tissues and cells. MTT assay was used to examine cell proliferation. Cell apoptosis was evaluated by detecting the apoptotic rate and the protein level of C-caspase 3 using flow cytometry and western blot assays. The protein levels of EMT-related proteins (E-cadherin, N-cadherin, and Vimentin) were measured by western blot. Cell migration and invasion were examined by transwell assay. Xenograft analysis was performed to explore the tumor growth in vivo. The binding sites of SNHG1 and miR-377-3p were predicted by the online software and confirmed by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay, and RNA pull-down assay. We found that SNHG1 was markedly upregulated in HCC tissues and cells. Knockdown of SNHG1 induced apoptosis and inhibited proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT) of HCC cells. SNHG1 knockdown suppressed the tumor growth of HCC in vivo. SNHG1 directly bound to miR-377-3p. Knockdown of miR-377-3p attenuated the effect of SNHG1 knockdown on proliferation, apoptosis, migration, invasion, and EMT of HCC cells. In conclusion, SNHG1 inhibited apoptosis and induced proliferation, migration, invasion, and EMT by sponging miR-377-3p in HCC, which indicated that SNHG1 may be a potential biomarker and therapeutic target for HCC treatment.