MicroRNA-487a promotes proliferation of esophageal cancer cells by inhibiting p62 expression

OBJECTIVE: MicroRNAs are endogenous, non-coding, small RNAs that can regulate biological processes. Previous studies have found that microRNA-487a serves as an oncogene. However, the role of microRNA-487a in esophageal cancer (EC) has not been reported. The aim of this investigation was to investigate the biological role of microRNA-487a in EC and its underlying mechanism. PATIENTS AND METHODS: The expression of microRNA-487a in 65 pairs of EC tissues and para-cancerous tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Chi-square test was used to analyze the relationship between microRNA-487a expression with age, sex, clinical stage and distant metastasis of OS patients. Kaplan-Meier survival analysis was conducted to evaluate the correlation between microRNA-487a expression and prognosis of EC patients. Subsequently, microRNA-487a expression in EC cell lines was detected as well. After microRNA-487a knockdown, cell counting kit-8 (CCK-8), EdU and tran-swell assay were conducted to evaluate the role of microRNA-487a in the biological performances of EC cells, respectively. Meanwhile, the apoptosis of EC cells was determined using flow cytometry. Finally, the interaction between microRNA-487a and p62 was explored by Western blot. Transwell assay was carried out in EC cells co-transfected with p62 overexpression plasmid and si-microRNA-487a. RESULTS: Compared with para-cancerous tissues, microRNA-487a expression was significantly higher in EC tissues, and the difference was statistically significant. MicroRNA-487a was highly expressed in EC cells as well. Low expression of microRNA-487a was positively correlated with clinical stage, whereas was not correlated with age, sex, lymph node metastasis and distant metastasis of EC patients. Kaplan-Meier survival curves showed that high expression of microRNA-487a was markedly associated with poor prognosis of EC. The knockdown of microRNA-487a significantly inhibited proliferative, migratory and invasive abilities of EC cells but induced cell apoptosis. Western blot results showed that the protein expression of p62 was remarkably upregulated after microRNA-478a knockdown in EC cells. Transwell assay demonstrated that co-transfection with overexpression plasmid of p62 and si-microR-NA-487a in EC cells markedly decreased invasive and migratory abilities. CONCLUSIONS: MicroRNA-487a is highly expressed in EC and is closely correlated with clinical stage and poor prognosis of EC. Our findings confirm that microRNA-487a promotes malignant progression of EC by regulating p62 expression.