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摘要
MicroRNAs (miRs) serve an essential role in tumorigenesis and are able to act as tumor suppressor genes or oncogenes. miR-106a has been identified generally as an oncogene in multiple types of human cancer; however, its association with osteosarcoma has not previously been understood. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect miR-106a expression in 18 osteosarcoma tissues compared with paired non-cancerous adjacent tissues as well as osteosarcoma cell lines (U2OS, Saos-2 and MG63) compared with a normal osteoblast cell line (hFOB1.19). The biological function of U2OS cells was assessed by using a Transwell cell invasion assay, MTS proliferation assay and flow cytometric analysis following the transfection with lentivirus-mediated small interfering RNA (miR-106a-inhibitor). Western blotting and Luciferase reporters were used to investigate whether VNN2 was a target of miR-106a in osteosarcoma cells. Based on the RT-qPCR data, miR-106a was significantly upregulated in osteosarcoma tissues and osteosarcoma cell lines compared with their control counterparts (P<0.01). The knockdown of miR-106a resulted in cell proliferation and invasion inhibition. Furthermore, apoptosis enhancement and G2/M cell cycle arrest were detected by flow cytometry. The western blot analysis indicated that U2OS cells infected with miR-106a-inhibitor lentivirus had a higher VNN2 protein expression level compared with cells infected with miR-106a-negative control lentivirus. Luciferase reporters containing the 3'-untranslated region sequence of VNN2 messenger RNA demonstrated VNN2 may be a target of miR-106a. In addition, a negative correlation was confirmed between the expression of VNN2 and miR-106a in the tumor samples. The results of the present study indicate that the knockdown of miR-106a overexpressed VNN2 to inhibiting the proliferation, migration and invasion as well as inducing the apoptosis of human osteosarcoma cells.
- 出版日期2018-10
- 单位中国医科大学
