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Mol Cell Biochem. 2009 Jul;327(1-2):257-66. doi: 10.1007/s11010-009-0064-y. Epub 2009 Feb 20.

Lentivirus-mediated RNAi knockdown of insulin-like growth factor-1 receptor inhibits growth, reduces invasion, and enhances radiosensitivity in human osteosarcoma cells.

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  • 1Department of Biochemistry and Molecular Biology, Nanjing Medical University, Hanzhong Road 140, 210029 Nanjing, Jiangsu Province, People's Republic of China.


The type 1 insulin-like growth factor receptor (IGF-1R) is essential for tumorigenicity, tumor proliferation, and protection from apoptosis. IGF-1R overexpression has been found in many human cancers including osteosarcoma. To explore its possibility as a therapeutic target for the treatment of osteosarcoma, lentivirus-mediated siRNA was employed to downregulate endogenous IGF-1R expression to study the function of IGF-1R in tumorigenesis and radioresistance of osteosarcoma cells. The IGF-1R expression was persistently and markedly reduced by lentivirus-mediated RNAi. Downregulation of IGF-1R expression in osteosarcoma cells significantly suppressed their growth rates in vitro and reduced the potential of tumorigenicity in vivo. Moreover, the specific downregulation arrested cells in G(0)/G(1) phase of cell cycle and also induced apoptosis which correlated with the activation of Caspase-3. Furthermore, we also observed that suppression of IGF-1R could reduce the invasiveness of osteosarcoma cells and enhance their radiosensitivity. Our study suggested that lentivirus-mediated RNAi silencing targeting IGF-1R could induce potent antitumor activity and radiosensitizing activity in human osteosarcomas.

[PubMed - indexed for MEDLINE]
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