IGF-I Receptor Inhibition Combined with Rapamycin or Temsirolimus Inhibits Neuroblastoma Cell Growth

Background: Neuroblastoma is the third most common solid tumor in children. Treatment continues to be challenging. The pathogenesis of neuroblastoma has been related to expression of the type 1 insulin-like growth factor receptor (IGF1R) and to transcription factor MYC-N amplification. Previous studies have shown that MYC-N expression is disrupted by blockade of the IGF1R with a specific monoclonal antibody, αIR3. Inhibition of IGF1R signaling can be accomplished by other agents, including rapamycin or temsirolimus, which target mTOR (mammalian target of rapamycin). Materials and Methods: BE-2(c) and IMR-32 neuroblastoma cell lines were treated with varying concentrations of αIR3, rapamycin and temsirolimus alone or in combination and the viable cells were counted. Results: Blockade of IGF1R signaling significantly inhibited cell growth as compared to untreated controls (p