Downregulation of 14-3-3β inhibits proliferation and migration in osteosarcoma cells.

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.