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.
MeSH terms
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Animals
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Breast Neoplasms / metabolism
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Breast Neoplasms / pathology*
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Enzyme Activation
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Female
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Gene Expression Regulation, Neoplastic
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Humans
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Integrin beta4 / physiology*
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JNK Mitogen-Activated Protein Kinases / metabolism
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Mammary Glands, Animal / metabolism
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Mammary Glands, Animal / pathology
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Mammary Glands, Human / metabolism
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Mammary Glands, Human / pathology
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Mammary Neoplasms, Animal / metabolism
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Mammary Neoplasms, Animal / pathology*
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Mice
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Mice, Transgenic
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Neoplasm Invasiveness
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Receptor, ErbB-2 / physiology*
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STAT3 Transcription Factor / metabolism
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Signal Transduction
Substances
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Integrin beta4
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STAT3 Transcription Factor
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Stat3 protein, mouse
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Receptor, ErbB-2
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JNK Mitogen-Activated Protein Kinases