Abstract: To investigate the effects of hsa-miR-223 on the migration and invasion capability of human esophageal cells, and to further explore its mechanism of action, which alters the biological function of esophageal carcinoma cells. Methods: The expression of miR-223 and Artemin (ARTN) in human esophageal carcinoma cell lines were determined using real-time polymerase chain reaction ( PCR ) and Western blot analysis. The stable cell line KYSE150, which overexpressed miR-223, was established through G418 screening. Wound healing and Boyden chamber assays were performed to analyze the migration and the invasion capabilities of the cells. Based on the changes in biological function, the mechanism of hsa-miR-223 involvement in migration and invasion was further studied using a dual-luciferase reporter assay and Western blot. Results: The results of real-time PCR indicated that hsa-miR-223 was downregulated in the esophageal carcinoma cell line KYSE150 with high metastatic potential, whereas ARTN was overexpressed in the KYSE150 cell line. The stable cell line KYSE-150 was successfully established. The wound healing assay and the Boyden chamber assay showed that the migration and invasion capability of KYSE-150 cell line were significantly suppressed. Moreover, the dual-luciferase reporter assay showed that miR-223 decreased the activity of luciferase in the stable KYSE150 cell line transfected with pMIR-ARTN. This was confirmed by the Western blot analysis, which indicated that miR-223 suppressed ARTN expression. Conclusion: Hsa-miR-223 is downregulated in the human esophageal carcinoma cell line KYSE150 with high metastatic potential. Acting as a tumor suppressor gene, hsa-miR-223 suppressed migration and invasion by targeting ARTN. ARTN is a potential therapeutic target for the biological treatment of tumors.