Abstract. microRNAs (miRNAs/miRs) are crucial regulators of gene expression at the post-translational level through promoting mRNA degradation or the repression of translation of target genes. miRs have been confirmed to serve a dominant role in tumor biology. miR-486-5p has been ascertained to be involved in non-small-cell lung cancer, breast cancer and hepatocellular carcinoma; however, the expression and function of miR-486-5p in esophageal squamous cell carcinoma (ESCC) has yet to be elucidated. The present study aimed to analyze the expression levels of miR-486-5p in ESCC tissues and paired normal adjacent tissues, and determine the effects of miR-486-5p on esophageal cancer cells using MTT, wound scratch and apoptosis assays. The current results showed that miR-486-5p was significantly downregulated in ESCC specimens. Ectopic expression of miR-486-5p by synthetic mimics reduced cell proliferation and migration and induced increased cell apoptosis. The results indicated miR-486-5p may function as a tumor suppressor in ESCC. The present study demonstrated that miR-486-5p was downregulated in ESCC and served a anti-oncogene role in ESCC via affecting cellular migration.

Abstract. MicroRNAs (miRs) are small endogenous non-coding RNAs that play a vital role in carcinogenesis. miR-193a-3p has been described in multiple cancers. However, the function of miR-193a-3p in esophageal squamous cell carcinoma (ESCC) is still unclear. To explore the role of miR-193a-3p in ESCC, reverse transcription-quantitative polymerase chain reaction was used to evaluate the expression of miR-193a-3p in 48 paired ESCC and adjacent normal tissues. In addition, the impact of miR-193a-3p on cell proliferation, migration and apoptosis were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, wound scratch assay and flow cytometry, respectively. The results revealed that miR-193a-3p was upregulated in ESCC, compared with adjacent normal tissues. Downregulation of miR-193a-3p expression using a synthesized inhibitor suppressed cell proliferation and migration, and induced cell apoptosis, indicating that miR-193a-3p could be characterized as an oncogene in ESCC. In summary, the present study demonstrated that miR-193a-3p was upregulated in ESCC, where it plays a significant role by affecting cellular proliferation, migration and apoptosis.