Objective  To explore the potential mechanism of long non-coding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1(MALAT1) in the progression of hepatocellular carcinoma (HCC) and chemotherapy resistance.

  Methods  This study included 20 pairs of tissues including HCC tissues and adjacent non-cancerous tissues (> 5 cm from cancerous tissues) from patients who underwent surgeries. The expressions of MALAT1, miR-618 and MAEL in tumor tissues and HCC cell lines were detected by fluorescence quantitative PCR (qRT-PCR). The upstream and downstream targets of miR-618 were predicted by bioinformatics and identified by luciferase assay. The function of MALAT1 in the proliferation of HCC was analyzed by cell viability, and the function of MALAT1 in HCC cell invasion and migration were studied by the analysis of invasion and scratch experiments. The effects of MALAT1, miR-618 and MAEL on the epithelial-mesenchymal transition (EMT) of HCC cells were analyzed by qRT-PCR and western blotting. MAEL's chemotherapy resistance research was verified by MTT method and clone formation assay.

  Results  Compared with adjacent tissues and liver cell lines, MALAT1 and MAEL were highly expressed in tumor tissues and HCC cell lines, and miR-618 was lowly expressed (P < 0.05). The dual luciferase assay determined that the upstream and downstream targets of miR-618 were MALAT1 and MAEL, respectively. The proliferation, invasion and migration of cells silencing MALAT1, overexpression of miR-618 or silencing MAEL decreased, the difference was statistically significant (P < 0.05). BMALAT1 regulated tumor EMT process by regulating miR-618/MAEL. MAEL promoted HCC resistance to epirubicin.

  Conclusion  LncRNA MALAT1 can regulate the expression of MAEL by competitively binding miR-618 to affect HCC progression and drug resistance. The EMT process plays an important role in the regulation of HCC biological functions by LncRNA MALAT1, which suggests that MALAT1 may be a potential therapeutic target for HCC treatment.