Autocrine secreted insulin-like growth factor-I stimulates MAP kinase-dependent mitogenic effects in human primitive neuroectodermal tumor/medulloblastoma.

R. Patti, C. D. Reddy, B. Geoerger, M. A. Grotzer, M. Raghunath, L. N. Sutton, P. C. Phillips

Research output: Contribution to journalArticlepeer-review

38 Scopus citations

Abstract

Primitive neuroectodermal tumors/medulloblastoma (PNET/MB) have similarities to neuroectodermal progenitor cells of the developing CNS. Since insulin-like growth factor I (IGF-I) exerts pleiotrophic effects on cells in the developing CNS, we evaluated the production, mitogenic effects and signaling pathways of IGF-I in PNET/MB cells and found that IGF-I is an autocrine growth factor in human PNET/MB cell lines tested. Stimulation of DAOY cells by IGF-I led to phosphorylation of its cognate receptor (IGF-IR) and resulted in cell proliferation. These effects of IGF-I were suppressed by IGF-IR blocking antibodies and by PD 98059, MAP kinase pathway inhibitor. The results demonstrate the existence of an autocrine IGF-I/IGF-IR loop and indicate that IGF-I promotes proliferation via MAP kinase pathway.

Original languageEnglish
Pages (from-to)577-584
Number of pages8
JournalInternational Journal of Oncology
Volume16
Issue number3
DOIs
StatePublished - Mar 2000
Externally publishedYes

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