Mucin 1 expression is regulated by hsa_circ_0055054/microRNA‑122‑5p and promotes hepatocellular carcinoma development

The abnormal expression of mucin 1 (MUC1) is a major cause of poor prognosis in patients with hepatocellular carcinoma (HCC). Competitive endogenous RNA demonstrates a novel regulatory mechanism that can affect the biological behavior of tumors. In the present study, the regulatory functions of hsa_circ_0055054 as well as those of microRNA (miR/miRNA) 122‑5p on MUC1 expression and its role in HCC cell proliferation, migration and invasion, were evaluated. MUC1 expression was assessed using western blotting and reverse transcription‑quantitative PCR. The phenotypic functions of the HCC cell lines were evaluated following MUC1 knockdown using Cell Counting Kit‑8, wound healing and Transwell assays. Bioinformatics tools were used to identify specific miRNAs and circular (circ)RNAs that interact with and can regulate MUC1. The stability of circRNAs was assessed using a Ribonuclease R assay. The binding of circRNA/miRNA/MUC1 was assessed using dual‑luciferase reporter assays and cellular function tests. Finally, in vivo experiments were performed using animal models. The results demonstrated that in MHCC97L cells, MUC1 and hsa_circ_0055054 were expressed at high levels while miR‑122‑5p was downregulated. The proliferation, migration and invasion of MHCC97L cells were suppressed by low MUC1 expression. hsa_circ_0055054 knockdown or miR‑122‑5p overexpression both led to a decrease in MUC1 expression. In MHCC97L cells with a low MUC1 expression caused by hsa_circ_0055054 knockdown, miR‑122‑5p inhibition resulted in the increased proliferation, migration and invasion of MHCC97L cells. In combination, the results of the present study indicate that hsa_circ_0055054 knockdown in MHCC97L cells leads to an increased expression of miR‑122‑5p and decreased expression of MUC1, which results in the inhibition of MHCC97L cell proliferation, migration and invasion.