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Open Access Propofol Inhibits Proliferation and Invasion of Osteosarcoma Cells by Regulation of MicroRNA-143 Expression

Propofol is one of the extensively commonly used intravenous anesthetic agents. Previous studies have indicated that propofol has the ability to influence the biological behavior of several human cancer cells. However, the effect of propofol on osteosarcoma and its related molecular mechanisms are still not clear. Here we found that propofol significantly elevated the expression of miR-143, inhibited cell proliferation and invasion, and promoted apoptosis in osteosarcoma cell line MG63. Propofol also efficiently decreased protein expression of matrix metalloproteinase 13 (MMP-13). Moreover, the overexpression of miR-143 decreased MMP-13 protein level. Finally, the neutralization of miR-143 by anti-miR-143 antibody reversed the effect of propofol on cell proliferation, apoptosis, and invasion and upregulated MMP-13 expression in MG63 cells. Taken together, propofol may have antitumor potential in osteosarcoma, which is partly due to the downregulation of MMP-13 expression by miR-143.

Keywords: Invasion; Matrix metalloproteinase 13 (MMP-13); Osteosarcoma; Proliferation; Propofol; miR-143

Document Type: Research Article

Affiliations: Department of Orthopedics, 161 Hospital of PLA, Huangpu Road, Wuhan, Hubei, China

Publication date: 25 April 2014

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  • Formerly: Oncology Research Incorporating Anti-Cancer Drug Design
    Oncology Research Featuring Preclinical and Clincal Cancer Therapeutics publishes research of the highest quality that contributes to an understanding of cancer in areas of molecular biology, cell biology, biochemistry, biophysics, genetics, biology, endocrinology, and immunology, as well as studies on the mechanism of action of carcinogens and therapeutic agents, reports dealing with cancer prevention and epidemiology, and clinical trials delineating effective new therapeutic regimens.

    From Volume 23, Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics is Open Access under the terms of the Creative Commons CC BY-NC-ND license.

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