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Tumor Biology |
Division of Neuroscience, Department of Neurology [J. Y. H. K., M. E. S., D. J. L., T. A. C., J. R. K., K. K. L., S. L. P.] and Department of Neurosurgery [L. C. G., L. G.], Children’s Hospital; Departments of Neurology [R. A. S.] and Surgery [J. W.], Division of Neurosurgery, The Brain Tumor Center, Beth Israel/Deaconess Medical Center; Departments of Pediatric Hematology-Oncology [J. Y. H. K., A. L. B.] and Microbiology and Molecular Genetics [C. D. S.], Dana-Farber Cancer Institute; and Division of Radiation Oncology, Massachusetts General Hospital [N. J. T.], Harvard Medical School, Boston, Massachusetts 02115; Department of Neurosurgery, New England Medical Center, Tufts School of Medicine, Boston, Massachusetts 02111 [J. W.]; and Division of Neuro-oncology, New York University Medical Center, New York, New York 10016 [J. C. A.]
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.
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