Abstract

Objective: To observe the impact of miR-32 on the proliferation and apoptosis of osteosarcoma U2OS cell line, and to explore its possible causative roles. Methods: Detection of miR-32 expression in carcinoma tissues and normal adjacent tissues of 44 osteosarcoma patients was achieved employing QRT-PCR technique. The liposome transfection technique was utilized to knock down the miR-32 of osteosarcoma U2OS cells and determine osteosarcoma cell proliferation, apoptosis migration ae well as invasion. Results: MiR-32 expressions in cancer tissues of osteosarcoma patients were markedly higher than that of adjacent tissues. Moreover, miR-32 expression further decreased as the clinical stage of the tumor progressed. MiR-32 knockdown could remarkably inhibit the formation of osteosarcoma cell clones, proliferation,migration and invasion level, whereas promote cancer cell apoptosis. Meanwhile, miR-32 knockdown can noteworthily reduce the level of oxidative stress and autophagy in osteosarcoma cells. Mechanistically, miR-32 can target and inhibit PTEN protein, knocking down miR-32 can activate PTEN/mTOR signaling pathway. In contrast, inhibiting PTEN protein expression can counteract the antitumor effect caused by miR-32 knockdown. Subcutaneous tumorigenesis experiments further confirmed the anti-osteosarcoma cell growth effect of miR-32. Conclusion: MiR-32 expression is apparently increased in cancer tissues of osteosarcoma patients. MiR-32 knockdown can suppress the proliferation of osteosarcoma cells and promote their apoptosis by targeting activation of PTEN-mediated mTOR activation.

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