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Signal transduction and oncogenesis by ErbB/HER receptors

Mina D Marmor1, Kochupurakkal Bose Skaria, Yosef Yarden

  • 1Department of Biological Regulation, The Weizmann Institute of Science, Rehovot, Israel.

International Journal of Radiation Oncology, Biology, Physics
|February 18, 2004
PubMed

Insights

Growth factors protect cells from radiation-induced death by activating ErbB receptors. Understanding ErbB signaling pathways is crucial for cancer therapy, especially concerning the oncogenic ErbB-2.

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Cancer Biology

Background:

  • Growth factors prevent apoptosis, a key cellular response to irradiation.
  • The epidermal growth factor (EGF) motif is central to a growth factor family that signals through ErbB receptors.
  • ErbB receptor tyrosine kinases mediate crucial cellular processes like proliferation, differentiation, and motility.

Purpose of the Study:

  • To review recent insights into ErbB receptor dimerization and signaling.
  • To discuss the regulation and dysregulation of ErbB signaling pathways in cancer.
  • To highlight therapeutic strategies targeting the ErbB network, particularly ErbB-2.

Main Methods:

  • Crystallographic analysis of receptor dimerization.
  • Review of signal transduction pathway activation and regulation.
  • Discussion of cancer-associated aberrant ErbB signaling.

Main Results:

  • Ligand-induced receptor dimerization and tyrosine kinase activation initiate signaling pathways.
  • The specific signaling outcome is determined by pathway complement, magnitude, and duration, influenced by ligand and receptor identity.
  • Dysregulation of the ErbB network is linked to various human cancers.

Conclusions:

  • ErbB receptor signaling is a complex network critical for normal cellular functions and implicated in cancer.
  • Structural insights into dimerization aid in understanding receptor activation.
  • Targeting the ErbB network, especially ErbB-2, offers therapeutic potential for cancer treatment.

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