Inhibition of IGF-I receptor signaling in combination with rapamycin or temsirolimus increases MYC-N phosphorylation

Don W. Coulter, Mary Beth Wilkie, Billie M. Moats-Staats

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Background: It has been previously shown that blockade of the type 1 insulin-like growth factor receptor (IGF1R) signaling combined with mTOR inhibition decreased neuroblastoma proliferation in vitro. MYC-N inactivation occurs through phosphorylation by downstream elements of the IGF1R signaling pathway. It was hypothesized that inhibition of IGF1R signaling would increase the inactivation of MYC-N. Materials and Methods: BE-2(c) and IMR-32 neuroblastoma cell lines were treated with varying concentrations of αIR3, rapamycin and temsirolimus either alone or in combination and the expression of MYC-N and phosphorylated MYC-N proteins were evaluated by Western blotting. The number of apoptotic cells was evaluated through cleaved caspase-3 expression. Results: IGF1R signaling blockade in combination with mTOR inhibition decreased MYC-N protein expression, increased MYC-N phosphorylation and significantly increased cleaved caspase-3 expression in treated cells. Conclusion: The combination of rapamycin or temsirolimus with αIR3 decreases MYC-N expression, increases MYC-N phosphorylation and induces apoptosis in vitro which may have clinical relevance to children with neuroblastoma.

Original languageEnglish (US)
Pages (from-to)1943-1949
Number of pages7
JournalAnticancer Research
Issue number6
StatePublished - Jun 2009


  • IGF-I receptor
  • Neuroblastoma
  • Phosphorylated MYC-N
  • Rapamycin
  • Temsirolimus
  • mTOR

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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