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This review summarizes recent findings that support a key role for the α6 integrins (α6β1 and α6β4) in the progression of breast carcinoma. The hypothesis that emerges from the existing data is that both of these integrins have the ability to sustain the survival of breast carcinoma cells, especially in stress conditions such as those that exist in the tumor microenvironment. The mechanisms by which these integrins promote survival appear to involve their ability to regulate the expression of vascular endothelial growth factor (VEGF), either at the level of transcription or translation. VEGF produced by breast carcinoma cells in response to α6 integrin regulation can function in an autocrine manner to promote survival signaling.
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Chung et al. (2004) studied this question.
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