LINC00355:8 promotes cell proliferation and migration with invasion via the MiR-6777-3p/Wnt10b axis in Hepatocellular Carcinoma

Background: Recent studies have reported that various long non-coding RNAs (lncRNAs) promote hepatocellular carcinoma (HCC) progression, and our previous study indicated that lncRNA LINC00355:8 is overexpressed in HCC. However, the role of LINC00355:8 in HCC is unclear. The primary aim of this study was to explore the biological role of LINC00355:8 in HCC. Methods: Microarray analysis was performed to explore the aberrantly expressed lncRNAs in HCC compared with precancerous tissues. Real-time PCR and in situ hybridization were used to investigate the expression of LINC00355:8 in HCC tissues. CCK8, EdU, colony formation, wound healing and transwell assays were performed to analyse cell proliferation, migration and invasion. A xenograft tumour model was established to analyse the effect of LINC00355:8 on tumour growth in vivo. Luciferase assays were utilized to explore the binding sites between miR-6777-3p and other genes, such as LINC00355:8 and Wnt10b. After cell transfection, the protein expression levels of Wnt10b, β-catenin, E-cadherin, N-cadherin, c-Myc and Snail were determined by Western blotting. Results: The present study revealed that LINC00355:8 was significantly upregulated in HCC, promoted HCC cell proliferation, migration and invasion in vitro and enhanced tumour growth in vivo. LINC00355:8 regulated miR-6777-3p expression by acting as a ceRNA, and the expression of Wnt10b was negatively modulated by miR-6777-3p. Moreover, LINC00355:8 could activate the Wnt/β-catenin signalling pathway and promote EMT progression by inhibiting the miR-6777-3p/Wnt10b interaction in HCC. Conclusion: Our findings indicate that LINC00355:8 activates Wnt10b and promotes HCC progression via the suppression of miR-6777-3p, which may provide novel therapeutic targets for HCC.