Long non-coding RNA TUG1 regulates the progression and metastasis of osteosarcoma cells via miR-140-5p/PFN2 axis

Z.-Y. Zhao, Y.-C. Zhao, W. Liu

Department of Osteoarthropathy, Yantaishan Hospital, Zhifu, Yantai, Shandong, China. huangcaideng9p3@126.com

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• Oncology

OBJECTIVE: Osteosarcoma (OS) is a frequently occurred tumor. Recently, increasing reports disclosed that long non-coding RNA taurine upregulated gene 1 (TUG1) was associated with OS development. Nevertheless, the precise regulatory pattern was not completely understood. Hence, we aimed to investigate the biological role of TUG1 in OS tumorigenesis.
PATIENTS AND METHODS: The levels of TUG1, microRNA-140-5p (miR-140-5p), and Profilin 2 (PFN2) were measured via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and the protein level of PNF2 was assessed using Western blot. In addition, MTT assay was employed to detect the ability of cell proliferation in MG63 and U2OS cells. Cell migration and invasion were estimated adopting transwell assay. Moreover, the Dual-Luciferase reporter assay was performed to verify the interrelation between miR-140-5p and TUG1 or PFN2.
RESULTS: TUG1 and PFN2 levels were evidently upregulated in OS tissues and cell lines. The knockdown of either TUG1 or PFN2 could restrain cell proliferation, migration, and invasion in OS cells. In addition, miR-140-5p was a target of TUG1 to regulate PFN2. The functions of PFN2 knockdown in cell behaviors were rescued after co-transfection with either miR-140-5p inhibitor or overexpression vector of TUG1. Importantly, TUG1 silencing could impede tumor progression in vivo.
CONCLUSIONS: TUG1 modulated cell proliferation, migration, and invasion via miR-140-5p/PFN2 axis in OS progression, which might trigger the development of therapeutic strategies for the treatment of OS.

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