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

Abstract

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.

• Authors: Kermit L Carraway 3rd, Colleen Sweeney
• Journal: Cancer cell (Cancer Cell) Vol. 10 Issue 2 Pg. 93-5 (Aug 2006) ISSN: 1535-6108 [Print] United States
• PMID: 16904607 (Publication Type: Journal Article, Review)

Chemical References

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

Topics

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