Novel agents targeting the IGF-1R/PI3K pathway impair cell proliferation and survival in subsets of medulloblastoma and neuroblastoma

PLoS One. 2012;7(10):e47109. doi: 10.1371/journal.pone.0047109. Epub 2012 Oct 8.

Abstract

The receptor tyrosine kinase (RTK)/phosphoinositide 3-kinase (PI3K) pathway is fundamental for cancer cell proliferation and is known to be frequently altered and activated in neoplasia, including embryonal tumors. Based on the high frequency of alterations, targeting components of the PI3K signaling pathway is considered to be a promising therapeutic approach for cancer treatment. Here, we have investigated the potential of targeting the axis of the insulin-like growth factor-1 receptor (IGF-1R) and PI3K signaling in two common cancers of childhood: neuroblastoma, the most common extracranial tumor in children and medulloblastoma, the most frequent malignant childhood brain tumor. By treating neuroblastoma and medulloblastoma cells with R1507, a specific humanized monoclonal antibody against the IGF-1R, we could observe cell line-specific responses and in some cases a strong decrease in cell proliferation. In contrast, targeting the PI3K p110α with the specific inhibitor PIK75 resulted in broad anti-proliferative effects in a panel of neuro- and medulloblastoma cell lines. Additionally, sensitization to commonly used chemotherapeutic agents occurred in neuroblastoma cells upon treatment with R1507 or PIK75. Furthermore, by studying the expression and phosphorylation state of IGF-1R/PI3K downstream signaling targets we found down-regulated signaling pathway activation. In addition, apoptosis occurred in embryonal tumor cells after treatment with PIK75 or R1507. Together, our studies demonstrate the potential of targeting the IGF-1R/PI3K signaling axis in embryonal tumors. Hopefully, this knowledge will contribute to the development of urgently required new targeted therapies for embryonal tumors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibodies, Monoclonal / pharmacology*
  • Antibodies, Monoclonal, Humanized
  • Apoptosis / drug effects
  • Blotting, Western
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Cell Survival / drug effects*
  • Humans
  • Medulloblastoma / metabolism*
  • Neuroblastoma / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Phosphoinositide-3 Kinase Inhibitors*
  • Receptor, IGF Type 1 / antagonists & inhibitors*
  • Receptor, IGF Type 1 / metabolism*
  • Signal Transduction / drug effects*

Substances

  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Phosphoinositide-3 Kinase Inhibitors
  • Receptor, IGF Type 1
  • teprotumumab

Grants and funding

This work was supported by grants from the Gottfried und Julia Bangerter-Rhyner-Stiftung, Schüller Stiftung, Frieda Locher-Hofmann-Stiftung, Huggenberger-Bischoff Stiftung zur Krebsforschung, Jubiläumsstiftung der Schweizerischen Mobiliar Genossenschaft, Fondation FORCE and the Department of Clinical Research of the University of Bern. The research leading to these results has received funding from the European Union's Seventh Framework Programme (FP7/2007–2013) under grant agreement n°259348. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.