Co-opted integrin signaling in ErbB2-induced mammary tumor progression

Cancer Cell. 2006 Aug;10(2):93-5. doi: 10.1016/j.ccr.2006.07.015.


Although almost two decades of study point to a central role for aberrant ErbB2 activation in breast cancer, many cellular and biochemical mechanisms underlying ErbB2-induced tumor initiation and progression remain to be resolved. A study by Guo et al. published recently in Cell indicates that the signaling function of beta4 integrin actively contributes to the initiation, growth, and invasion of ErbB2-induced mammary tumors in transgenic mice by promoting the activation of c-Jun and STAT3. These observations offer novel mechanistic insight into ErbB2 action and highlight the notion that ErbB2 co-opts the functions of other signaling proteins to elicit tumor progression.

Publication types

  • Review

MeSH terms

  • Animals
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / pathology*
  • Enzyme Activation
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Integrin beta4 / physiology*
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Mammary Glands, Animal / metabolism
  • Mammary Glands, Animal / pathology
  • Mammary Glands, Human / metabolism
  • Mammary Glands, Human / pathology
  • Mammary Neoplasms, Animal / metabolism
  • Mammary Neoplasms, Animal / pathology*
  • Mice
  • Mice, Transgenic
  • Neoplasm Invasiveness
  • Receptor, ErbB-2 / physiology*
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction


  • Integrin beta4
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • Receptor, ErbB-2
  • JNK Mitogen-Activated Protein Kinases