Long non-coding RNA HOXA11-AS accelerates cell proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma by modulating the miR-506-3p/Slug axis

Hepatocellular carcinoma (HCC) is an aggressively malignant type of cancer with a complex pathogenesis. Multiple studies have identified that lncRNA HOXA11-AS is involved in the development of HCC. Nevertheless, the pathological mechanisms of HOXA11-AS in the development of HCC require further investigation. In the present study, the role and underlying mechanisms of HOXA11-AS in HCC were examined. RT-qPCR revealed that HOXA11-AS expression was increased, while that of miR-506-3p was decreased in HCC tissues and cells compared with that in adjacent non-tumor tissues and normal hepatic cells. Dual-luciferase reporter assay and RNA pull-down assay indicated that HOXA11-AS directly interacted with miR-506-3p. miR-506-3p downregulation reversed the inhibitory effects of HOXA11-AS deletion on cell proliferation, invasion and epithelial-mesenchymal transition (EMT), as shown by CC K-8 and Transwell assays, as well as western blot analysis. Bioinformatics analysis and dual-luciferase reporter assay indicated that Slug was a target gene of miR-506-3p. The overexpression of Slug reversed the effects of HOXA11-AS deletion on the viability, invasion and the EMT of HCC cells. Taken together, the present study demonstrates that HOXA11-AS functions as an oncogene to promote the progression of HCC via the miR-506-3p/Slug axis, providing a therapeutic target for patients with HCC.