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Interfering with the interaction between ErbB1, nucleolin and Ras as a potential treatment for glioblastoma

Yona Goldshmit1, Sari Schokoroy Trangle2, Yoel Kloog3

  • 1Department of Neurobiology, Tel-Aviv University, Ramat-Aviv, Israel. Australian Regenerative Medicine Institute, Monash University, Australia. These authors contributed equally to this work.

Oncotarget
|September 28, 2014
PubMed

Insights

Targeting oncogenes Ras and nucleolin together inhibits cancer growth. Combined inhibition of Ras and nucleolin reduces tumor formation and proliferation, offering a new therapeutic strategy for cancers driven by these oncogenes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Three key oncogenes, ErbB receptors, Ras proteins, and nucleolin, are implicated in malignant transformation.
  • Nucleolin interacts with both Ras proteins and ErbB receptors.
  • Crosstalk among these proteins promotes anchorage-independent growth and tumor development.

Purpose of the Study:

  • To investigate the combined effect of Ras and nucleolin inhibitors on ErbB1 receptor-induced oncogenesis in U87-MG cells.
  • To elucidate the role of nucleolin in ErbB1 receptor activation by its ligand.
  • To evaluate the therapeutic potential of targeting both Ras and nucleolin in cancer treatment.

Main Methods:

  • Treatment of U87-MG cells with Ras and nucleolin inhibitors.
  • Assessment of cell death, proliferation, and migration.
  • Analysis of epidermal growth factor (EGF)-induced ErbB1 receptor activation and downstream signaling.
  • In vitro and in vivo evaluation of tumorigenicity.

Main Results:

  • Combined Ras and nucleolin inhibition reduced the oncogenic effects of ErbB1 receptor, enhancing cell death and reducing proliferation and migration.
  • Nucleolin inhibition blocked EGF-induced ErbB1 receptor activation and downstream signaling.
  • Ras inhibition (Salirasib) reduced cell viability and motility.
  • The combined treatment additively decreased tumorigenicity both in vitro and in vivo.

Conclusions:

  • Nucleolin plays a critical role in ErbB1 receptor activation.
  • Targeting both nucleolin and Ras concurrently offers a promising therapeutic strategy for cancers, including glioblastoma, driven by these oncogenes.
  • Combined inhibition of Ras and nucleolin additively reduces cancer cell proliferation, migration, and tumorigenicity.

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