Objective: To investigate the expression of long non-coding RNA MIF-AS1 (lncRNA MIF-AS1) in hepatocellular carcinoma (HCC) and its significance.   
Methods: The expressions of lncRNA MIF-AS1 in 94 paired specimens of HCC and adjacent tissue, and in different types of HCC cell lines and normal hepatic cells were detected by qRT-PCR. The relations of lncRNA MIF-AS1 expression with the clinicopathologic variables and prognosis of the patients were analyzed. The HCC cells were transfected with lncRNA MIF-AS1 interference sequences (silence group), lncRNA MIF-AS1 mimics (overexpression group) or negative control sequences (control group) respectively, and then, the changes in proliferative and invasion abilities as well as the protein expressions of epithelial–mesenchymal transition (EMT)-related molecules were examined.
Results: The lncRNA MIF-AS1 expression in HCC tissue was significantly higher than that in adjacent tissue, and in each studied HCC cell lines was significantly higher than that in normal hepatic cells (all P<0.05). The lncRNA MIF-AS1 expression was significantly associated with the serum AFP level, tumor size, portal vein microthrombus and TNM stage (all P<0.05). The tumor-free survival and overall survival rates in patients with high lncRNA MIF-AS1 expression were significantly lower than those with low lncRNA MIF-AS1 expression (both P<0.05). The lncRNA MIF-AS1 expression was an independent risk factor for both tumor-free survival and overall survival rates of the patients (both P<0.05). Results of cell experiment showed that compared with control group, the proliferative and invasion abilities were significantly reduced, and the protein expression of the epithelial phenotype molecule E-cadherin expression was increased, while the expressions of the mesenchymal phenotype molecules N-cadherin and vimentin were decreased in silence group (all P<0.05); the proliferative and invasion abilities were significantly enhanced, and the protein expression of E-cadherin expression was decreased, while the expressions of N-cadherin and vimentin were increased in overexpression group (all P<0.05).
Conclusion: The expression of lncRNAMIF-AS1 is up-regulated in HCC, and its expression level is closely related to malignant clinicopathologic features and poor prognosis of the HCC patients. The action mechanism of lncRNAMIF-AS1 may probably be related to its promoting EMT process.