1. Co-opted integrin signaling in ErbB2-induced mammary tumor progression.
- Author
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Carraway KL 3rd and Sweeney C
- Subjects
- Animals, Breast Neoplasms metabolism, Enzyme Activation, Female, Gene Expression Regulation, Neoplastic, Humans, 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, Mice, Mice, Transgenic, Neoplasm Invasiveness, STAT3 Transcription Factor metabolism, Signal Transduction, Breast Neoplasms pathology, Integrin beta4 physiology, Mammary Neoplasms, Animal pathology, Receptor, ErbB-2 physiology
- 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.
- Published
- 2006
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