IGF-1 receptor contributes to the malignant phenotype in human and canine osteosarcoma.

作者: E. Gregory MacEwen , Josep Pastor , Jonathan Kutzke , Rachel Tsan , Ilene D. Kurzman

DOI: 10.1002/JCB.20046

关键词:

摘要: To further define the role of insulin-like growth factor-1 (IGF-1) and its receptor (IGF-1R) in osteosarcoma (OS), human OS cell lines with low (SAOS-2) high (SAOS-LM2) metastatic potential three canine OS-derived were studied. Cell evaluated for: IGF-1R expression; expression IGF binding proteins (IGFBPs); effect IGF-1 on tumor growth, invasion, urokinase plasminogen activator (uPA), soluble uPA (suPAR), and; ectopic orthotopic tumorigenicity cells athymic mice. All exhibited steady-state mRNA IGF-1R. The SAOS-2 SAOS-LM2 expressed 9,138 10,234 cell-associated sites, respectively. Canine from 1,728 to 3,883 sites. Two IGF-1-treated displayed enhanced proliferation. formed colonies semisolid media, increased colony number. Matrigel invasion was one line following treatment. suPAR unchanged treatment, but highly five times more compared parental, SAOS-2. IGFBP-5 detected four lines, IGFBP-3 two lines. tumorigenic, metastasized spontaneously. In conclusion, express IGF-1R, which can contribute their invasion. There is suggestive evidence that increasing number may vivo tumorigenesis. Additional studies are needed determine how IGF-1/IGF-1R interactions malignant phenotype OS.

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