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- W2074022052 abstract "Neuroblastoma is a heterogeneous tumor consisting of N (neuronal) and S (stromal) cells. We report that more tumorigenic and motile N cells express higher levels of IGF-I receptor (IGF-IR) than less tumorigenic, more adherent S cells. Shc, one of the two major docking partners of IGF-IR, is equally expressed in N and S cell lines. IGF-I treatment phosphorylates Shc in N cells, but only weakly activates Shc in S cells. Expression of the second partner, insulin receptor substrate (IRS), is cell type specific. S cells exclusively express IRS-1 that undergoes sustained phosphorylation by IGF-I. In contrast, N cells express IRS-2 that is transiently phosphorylated by IGF-I. Downstream of IRS-2 and Shc, IGF-I treatment results in strong activation of Akt and MAPK in N cells and activation of both pathways is required for IGF-I-mediated differentiation. Only IGF-IR activation of phosphatidylinositol-3 kinase is required for tumor edge ruffling in N and S cells, with stimulation of focal adhesion kinase (FAK) and paxillin. This detailed understanding of the 'biochemical signature' of N and S cells provides the background needed to target and disrupt specific IGF signaling pathways in an attempt to develop more effective therapies." @default.
- W2074022052 created "2016-06-24" @default.
- W2074022052 creator A5056304003 @default.
- W2074022052 creator A5076914961 @default.
- W2074022052 creator A5089009468 @default.
- W2074022052 date "2004-01-08" @default.
- W2074022052 modified "2023-10-14" @default.
- W2074022052 title "Insulin-like growth factor-I signaling in human neuroblastoma cells" @default.
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- W2074022052 doi "https://doi.org/10.1038/sj.onc.1206924" @default.
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