Our previous study indicated that Aurora-B is involved in osteosarcoma (OS) cell invasion and metastasis; however, the mechanism underlying Aurora-B overexpression in OS remains unknown. In the present study, significantly downregulated let-7i expression in OS tissues and OS cells was observed compared with that in normal adjacent tumorous tissues and human osteoblast cell lines. Bioinformatic predictions have revealed a conserved binding site in a microRNA locus on Aurora‑B, suggesting the potential of let‑7i targeting the Aurora‑B gene. To validate this, a luciferase reporter assay was performed on OS cells. The results indicated that Aurora‑B is a likely to be a direct target negatively regulated by let‑7i. The expression of let‑7i in OS cells was restored by infection with let‑7i mimics. Results revealed that Aurora‑B mRNA and protein expression levels were significantly decreased. Furthermore, the proliferation, migration and invasion abilities of OS cells were significantly suppressed by infection with let‑7i mimics. Notably, the inhibitory effect of silencing Aurora‑B by LV‑shAurora‑B on cell proliferation, migratory and invasive ability was significantly lower than that by let‑7i mimics, which indicated that let‑7i inhibits cell malignant phenotypes partially by targeting Aurora‑B in OS cells. All data suggested that let‑7i may be a novel potential target for OS treatment.