IMR Press / FBL / Volume 12 / Issue 13 / DOI: 10.2741/2433

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

IFI16 inhibits tumorigenicity and cell proliferation of bone and cartilage tumor cells
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1 Department of Orthopaedic Surgery, New York University School of Medicine, New York, New York 10003, USA
2 Department of Cell Biology, New York University School of Medicine, New York, New York 10016, USA
3 Institute of Pathogenic Biology, Shandong University School of Medicine, Jinan, Shandong, P.R. China
4 Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT 06520, USA
Front. Biosci. (Landmark Ed) 2007, 12(13), 4855–4863;
Published: 1 September 2007

IFI16 is a member of the interferon-inducible p200-protein family, capable of modulating cell proliferation, and cellular senescence. In this study, these effects of IFI16 were studied in tumor cells derived from bone and cartilage. The level of IFI16 was markedly lower in human osteosarcomas as compared with its level in normal bone. Overexpression of functional IFI16 in human osteosarcoma and chondrosarcoma cell lines markedly inhibited colony formation, and significantly inhibited cell growth, an effect that could be reversed by introduction of gene specific siRNA into tumor cells. These inhibitory effects of IFI16 were associated with upregulation of p21 and inhibition of cyclin E, cyclin D1, c-Myc and Ras. In addition, ectopic expression of IFI16 in tumor cells increased senescence-associated beta-galactosidase and induced a senescence-like phenotype. In view of such effects, IFI16 might be a suitable target for therapeutic intervention in osteosarcoma and chondrosarcoma.

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