Long non-coding RNA 01559 mediates the malignant phenotypes of hepatocellular carcinoma cells through targeting miR-511

•High expression of LINC01559 was uncovered and resulted in an unfavorable prognosis in HCC.•Downregulation of LINC01559 obstructed the proliferation and growth of HCC cells.•LINC01559 acted as a molecule sponge for miR-511.•LINC01559 regulated SLC38A1 expression by competitively interaction with miR-511.•miR-511 downregulation reversed the suppressive effect of LINC01559-knockdown on HCC cells proliferation, invasion and migration. Long non-coding RNA 01559 (LINC01559) has been found to be associated with the tumorigenesis of malignant tumors. However, the expression pattern and the potential molecular mechanism of LINC01559 in hepatocellular carcinoma (HCC) progression remain unclear. Expression profile and clinical data of patients with HCC were retrieved from The Cancer Genome Atlas database. The quantitative real-time PCR (qRT-PCR) and western blot assays were used to detect the mRNA and protein levels of indicated molecules. Loss-of-function of LINC01559 and microRNA-511 (miR-511) assays were implemented to validate their roles in regulating proliferation, invasion and migration of HCC HepG2 and Huh7 cells. Bioinformatics and luciferase reporter assays were used to determine the possible interactions between LINC01559, miR-511 and solute carrier family 38 member 1 (SLC38A1). LINC01559 was highly expressed, and related to poor prognosis in HCC patients. LINC01559-knockdown restrained the proliferation and growth of HepG2 and Huh7 cells. Furthermore, LINC01559 can function as a sponge for miR-511, which was downregulated in HCC patients. Downregulation of miR-511 significantly increased the cell viability, invasive and migratory capacities, and could abolish the suppressive effect of LINC01559-knockdown on these HCC cells. Moreover, SLC38A1 was a target of miR-511 and upregulated in HCC. Knockdown of LINC01559 significantly reduced while miR-511 inhibitor notably elevated the mRNA and protein levels of SLC38A1, which were abrogated by downregulation of LINC01559 and miR-511 simultaneously. LINC01559 functioned as a competitive endogenous RNA mediating the malignant phenotypes of HCC cells via sponging miR-511, and may be a considerable therapeutic bio-target in HCC.