Activation of neurotrophin-3 receptor TrkC induces apoptosis in medulloblastomas

Cancer Res. 1999 Feb 1;59(3):711-9.

Abstract

Elevated expression of the neurotrophin-3 (NT-3) receptor TrkC by childhood medulloblastomas is associated with favorable clinical outcome. Here, we provide evidence that TrkC is more than simply a passive marker of prognosis. We demonstrate that: (a) medulloblastomas undergo apoptosis in vitro when grown in the presence of NT-3; (b) overexpression of TrkC inhibits the growth of intracerebral xenografts of a medulloblastoma cell line in nude mice; and (c) trkC expression by individual tumor cells is highly correlated with apoptosis within primary medulloblastoma biopsy specimens. TrkC-mediated NT-3 signaling promotes apoptosis by activating multiple parallel signaling pathways and by inducing immediate-early gene expression of both c-jun and c-fos. Considered collectively, these results support the conclusion that the biological actions of TrkC activation affect medulloblastoma outcome by inhibiting tumor growth through the promotion of apoptosis.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism
  • Child, Preschool
  • Enzyme Activation
  • Female
  • Humans
  • Infant
  • Male
  • Medulloblastoma / enzymology
  • Medulloblastoma / pathology*
  • Medulloblastoma / ultrastructure
  • Mice
  • Mice, Nude
  • Nerve Growth Factors / pharmacology
  • Neurotrophin 3
  • Phosphatidylinositol 3-Kinases / metabolism
  • Prognosis
  • Proto-Oncogene Proteins c-fos / genetics
  • Proto-Oncogene Proteins c-fos / metabolism
  • Receptor Protein-Tyrosine Kinases / biosynthesis
  • Receptor Protein-Tyrosine Kinases / metabolism
  • Receptor Protein-Tyrosine Kinases / physiology*
  • Receptor, trkC
  • Receptors, Nerve Growth Factor / biosynthesis
  • Receptors, Nerve Growth Factor / metabolism
  • Receptors, Nerve Growth Factor / physiology*
  • Signal Transduction / physiology
  • Stimulation, Chemical
  • Tumor Cells, Cultured

Substances

  • Nerve Growth Factors
  • Neurotrophin 3
  • Proto-Oncogene Proteins c-fos
  • Receptors, Nerve Growth Factor
  • Phosphatidylinositol 3-Kinases
  • Receptor Protein-Tyrosine Kinases
  • Receptor, trkC
  • Calcium-Calmodulin-Dependent Protein Kinases