Insulin-like growth factor I stimulates motility in human neuroblastoma cells

Oncogene. 2001 Nov 8;20(51):7542-50. doi: 10.1038/sj.onc.1204927.


Motility is an important process that contributes to cancer cell spread. Growth factors are key regulators of motility in many cell types. Insulin-like growth factor I (IGF-I) causes SH-SY5Y human neuroblastoma cells to undergo dynamic morphological changes, leading to the extension of lamellipodia. IGF-I stimulated lamellipodia extension requires signaling through both phosphatidylinositol 3-kinase (PI3-K) and MAP kinase pathways. IGF-I, over a period of hours, stimulates SH-SY5Y and SHEP neuroblastoma cells to become more motile. While SH-SY5Y and SHEP cells use different insulin receptor substrate (IRS) isoforms to transduce signals from the IGF-I receptor, IGF-I has the same relative effect on the motility of both cell lines. Blocking the PI3-K and MAP kinase pathways attenuates the ability of IGF-I to increase motility. Overexpression of PTEN also attenuates IGF-I mediated motility. These results delineate some of the proximal events in the signaling mechanism utilized by IGF-I to stimulate cell motility.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Cell Division
  • Cell Line
  • Cell Movement
  • Culture Media, Serum-Free
  • Dose-Response Relationship, Drug
  • Humans
  • Immunoblotting
  • Insulin-Like Growth Factor I / metabolism*
  • Insulin-Like Growth Factor I / physiology*
  • MAP Kinase Signaling System
  • Microscopy, Video
  • Neuroblastoma / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Precipitin Tests
  • Protein Isoforms
  • Pseudopodia / metabolism
  • Signal Transduction
  • Time Factors
  • Tumor Cells, Cultured


  • Culture Media, Serum-Free
  • Protein Isoforms
  • Insulin-Like Growth Factor I
  • Phosphatidylinositol 3-Kinases