Abstract
Increasing evidence has demonstrated that microRNAs (miRNAs or miRs) are involved in cancer initiation and progression. Previous studies have indicated that miR-221 is one of the most consistently overexpressed miRNAs in multiple types of cancer. However, the role of miR-221 in osteosarcoma carcinogenesis and progression is not yet fully understood. Thus, the aim of the present study was to examine the expression of miR-221 in osteosarcoma and to determine the effects of miR-221 on the biological behavior of osteosarcoma cells. RT-qPCR revealed that the expression of miR-221 was significantly upregulated in the osteosarcoma tissues and osteosarcoma cell lines (p<0.05). In order to explore the role of miR-221 in osteosarcoma, the expression of miR-221 in the human osteosarcoma cell line MG‑63 was upregulated or downregulated by transfection with miR-221 mimic or miR-221 inhibitor, respectively. The results from RT-qPCR revealed that we had successfully generated MG‑63 cells in which miR-221 was either overexpressed or depleted. To investigate the effects of miR-221 on osteosarcoma cell proliferation, invasion and migration, a tetrazolium-based colorimetric assay, propidium iodide (PI) staining, a transwell migration assay and a wound healing assay were used in the present study. The results revealed that the proliferation, invasion and migration ability of the MG‑63 cells in which miR-221 was overexpressed was enhanced, and the proliferation, invasion and migration ability of the MG‑63 cells in which miR-221 was depleted was suppressed. The correlation between miR-221 and phosphatase and tensin homolog (PTEN) expression was investigated by RT-qPCR and western blot analysis. The results revealed that the downregulation of miR-221 significantly increased the expression of PTEN, whereas the upregulation of miR-221 significantly reduced the expression of PTEN. Taken together, our results suggest that miR-221 enhances the proliferation, invasion and migration ability of osteosarcoma cells partly by suppressing PTEN.
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