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  • Title: Induction of N-myc in neuroblastoma by autocrine IGF-II depends on farnesylated Ras. Application of farnesyltransferase inhibitors.
    Author: Wittrock J, Schweizer P, Girgert R.
    Journal: Anticancer Res; 2002; 22(6C):4205-9. PubMed ID: 12553057.
    Abstract:
    Genetic aberrations are the primary events leading to carcinogenesis in various tissues and are characteristic for certain tumor types. Amplification of N-myc and deletion of 1p significantly correlate with poor prognosis of neuroblastoma patients. Very little informations is available on the regulation of N-myc expression by external factors. Insulin-like growth factor-II (IGF-II) has been identified as an autocrine growth factor in neuroblastoma. Four neuroblastoma cell lines were examined for their expression of IGF-II and IGF-receptor. Stimulation of neuroblastoma cells with IGF-II leads to an increased activity of the MAP-kinase Erk1, an induction of N-myc expression and an enhanced proliferation rate. In order to disrupt the signal transduction of the IGF-receptor, we inactivated the Ras-proteins in neuroblastoma cells by inhibition of the farnesyl-protein transferase by FTI-277. This inactivation prevented activation of MAP-kinase Erk1 and induction of N-myc expression by IGF-II. Inactivation of Ras by farnesyltransferase inhibitors might become a promising new approach in future treatments of neuroblastoma tumors.
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