Expression of miR-664 and miR-184 on proliferation, apoptosis and migration of osteosarcoma cells.

The expression of micro-ribonucleic acid miR-664 and miR-184 on the biological characteristics of osteosarcoma (OS) SOSP-9607 cells was investigated. Eighteen surgical specimens of OS and 18 normal tissue specimens were collected. The expression of miR-664 and miR-184 was detected via fluorescence reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The OS cell line SOSP-9607 was selected as the object of study, and miR-664 blank group, miR-664 mimic group, miR-664 inhibitor group, miR-184 blank group, miR-184 mimic group and miR-184 inhibitor group were established through transfection. Changes in apoptosis were detected via flow cytometry, the cell proliferation capacity was detected via Cell Counting Kit-8 assay, and the cell migration was observed via wound healing assay. In cancer tissues of OS patients, the relative expression of miR-664 and miR-184 was significantly higher than that in para-carcinoma tissues (P<0.05). The cell growth in miR-664 inhibitor group was obviously decreased compared with those in miR-664 blank and mimic groups (P<0.05). There were differences in the cell migration capacity among groups (P<0.01), and the cell scratch areas in miR-664 and miR-184 mimic groups were significantly decreased compared with those in miR-664 and miR-184 blank groups (P<0.05), while they were significantly increased in miR-664 and miR-184 inhibitor groups compared with those in miR-664 and miR-184 blank and mimic groups (P<0.05, P<0.01). There were differences in the apoptosis rate among groups (P<0.01) and apoptosis in miR-664 and miR-184 inhibitor groups was remarkably increased compared with those in miR-664 and miR-184 blank and mimic groups (P<0.05). Downregulating the expression of miR-664 and miR-184 may promote apoptosis, inhibit the proliferation and reduce the migration capacity of SOSP-9607 cells. Therefore, miR-664 and miR-184 may provide a theoretical basis for the target selection in clinical targeted therapy and drug development for OS.