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.

Activin A is a member of the TGF‑β superfamily. Previous studies have demonstrated that activin A exhibited pluripotent effects in several tumours. However, the roles of activin A signaling in osteosarcoma pathogenesis have not been previously investigated. Therefore, the present study aimed to investigate the effects of activin A on osteosarcoma cell proliferation, invasion and migration. Firstly, the expression of activin A in osteosarcoma cell lines (MG63, SaOS‑2 and U2OS) and a human osteoblastic cell line (hFOB1.19) was detected using reverse transcription quantitative polymerase chain reaction and western blotting. Activin A was upregulated in osteosarcoma cell lines compared with hFOB1.19 cells. To investigate the effects of activin A on osteosarcoma cell proliferation, invasion and migration, MG63 cells were generated in which activin A was either overexpressed or depleted. MTT staining, propidium iodide staining and a Transwell assay were used to analyze the cell cycle, proliferation, invasion and migration of MG63 cells, respectively. The results of the present study revealed that the abilities of proliferation, invasion and migration were suppressed in MG63 cells in which activin A was depleted, while they were enhanced in activin A-overexpressing cells. In conclusion, the results of the present study suggested that activin A may facilitate proliferation, invasion and migration of osteosarcoma cells, and it may therefore be a potential target for the treatment of osteosarcoma.

The 14-3-3 protein isoform β (14‑3‑3β), which is an intracellular adaptor protein that exists in all eukaryotic organisms, is highly expressed in many cancer tissues, including glioma, lung carcinoma and breast cancer. However, 14‑3‑3β expression and function in osteosarcoma progression remain unknown. In the present study, the endogenous expression of 14‑3‑3β was assessed in osteosarcoma samples and the effect of 14‑3‑3β knockdown was examined in human osteosarcoma MG63 cells using small interfering RNA (siRNA). mRNA and protein expression levels for 14‑3‑3β were detected by reverse transcription‑quantitative polymerase reaction and western blotting, respectively. The results demonstrated that endogenous 14‑3‑3β mRNA and protein were highly expressed in human osteosarcoma tissues and osteosarcoma cell lines (U2OS, MG63 and SaOs‑2), but not in normal bone tissues or normal osteoblast hFOB1.19 cells. These data suggested that increased expression of 14‑3‑3β may be significantly associated with the development and progression of osteosarcoma. Therefore, the effect of 14‑3‑3β knockdown in MG63 cells was further examined in vitro. Knockdown of 14‑3‑3β by siRNA significantly decreased cell viability, and inhibited cell proliferation and invasion. In addition, 14‑3‑3β knockdown significantly decreased the protein expression levels of β‑catenin, cyclin D1, v‑myc avian myelocytomatosis viral oncogene homolog and matrix metallopeptidase 9 in osteosarcoma MG63 cells. These results suggested that the anticancer effects of 14‑3‑3β knockdown in MG63 cells might be mediated by the inhibition of the Wnt/β‑catenin signaling pathway. In summary, 14‑3‑3β knockdown decreased proliferation and invasion in MG63 cells, which suggests a potential therapeutic application for 14‑3‑3β as a novel target for the treatment of osteosarcoma patients.

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