Abstract
Numerous studies have elucidated the impact of long non‑coding (lnc)RNAs in carcinogenesis; however, the role and the mechanism of the lncRNA LOC284454 in hepatocellular carcinoma (HCC) remain unknown. In the present study, reverse transcription‑quantitative PCR assay, χ2 analysis and Kaplan‑Meier analysis were performed to assess the role of LOC284454 in HCC. Furthermore, MTT and Transwell assays were performed to measure the function of LOC284454 on HCC cell proliferation, invasion and migration. RNA immunoprecipitation, chromatin immunoprecipitation, RNA pull‑down, fluorescence in situ hybridization and luciferase reporter assays were performed to explore the mechanism of LOC284454. The results revealed that LOC284454 expression was aberrantly elevated in HCC and increased LOC284454 expression was markedly associated with aggressive clinicopathological factors and shorter survival time in patients with HCC, suggesting that LOC284454 behaved as an oncogenic factor in HCC. Mechanistically, LOC284454 could bind with the enhancer of zeste homolog 2 (EZH2) mRNA and subsequently inhibit E‑cadherin expression by binding to its promoter region. The rescue assay demonstrated that E‑cadherin was essential for the oncogenic function of LOC284454 in HCC cells. The present results suggested that the LOC284454/EZH2/E‑cadherin axis may be an alternative therapeutic target for patients with HCC.