China Oncology ›› 2013, Vol. 23 ›› Issue (4): 285-291.doi: 10.3969/j.issn.1007-3969.2013.04.008

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miR-96 expression in osteosarcoma and the role in cell proliferation and apoptosis

WU De-ming, LIU Xiang, JIANG Chuan, DAI Min   

  1. Department of Orthopaedics, the First Affiliated Hospital of Nanchang University, Nanchang Jiangxi 330006, China
  • Online:2013-04-25 Published:2014-11-19
  • Contact: DAI Min E-mail: leizhen6677@163.com

Abstract:

Background and purpose: MicroRNAs are small non-coding endogenous RNA molecules that can inhibit protein translation partly through binding with target mRNAs. MiR-96 is over expressed in many kinds of human tumor cells. The present study aimed to investigate the expression of miR-96 in osteosarcoma tissues and demonstrate its role in osteosarcoma cell lines proliferation, cell cycle and apoptosis. Methods: The expressions of miR-96 in 40 pairs of osteosarcoma and their adjacent nontumorous tissues were detected by TagMan MGB probe method. The antisense technology was used to decrease the expression of miR-96 in osteosarcoma cells (U2-OS, MG-63), MTT assay and flow cytometry were performed to investigate the effect of miR-96 on the cell proliferation, cell cycles and apoptosis. Results: We examined miR-96 expression levels in 40 pairs of human osteosarcoma and their corresponding nontumorous tissues. miR-96 was found to be over-expressed in 62.5% (25/40) of the osteosarcoma cases (P<0.05). The cell growth ability of U2-OS and MG-63 cells was significantly inhibited following transfection of antisense-microRNA-oligonucleotides-96 (AMO-miR-96). U2-OS and MG-63 cells were mainly detained in G0/G1, and the percentage of cells at S and G2/M decreased. In addition, knocking down the expression of miR-96 in U2-OS and MG-63 cells resulted in an increase in early apoptosis. Conclusion: miR-96 is over-expressed in human osteosarcoma. Inhibition of miR-96 expression can not only effectively suppress the growth of U2-OS and MG-63 cells, but also induce cell apoptosis. MiR-96 may serve as a new molecular target for the regulation of gene expression in osteosarcoma.

Key words: Osteosarcoma, miR-96, Antisense oligonucleotides