Genomic mechanisms

Classically, the ER functions as a transcription factor within the nucleus, and the ability of estrogen/antiestrogens to regulate gene expression has been extensively investigated in experimental models of human breast cancer both in vitro and in vivo. Based on these studies, it is becoming increasingly evident that estrogens can promote the autocrine expression of growth factor signaling pathway elements (Figure 10.2, 2a)44,45 - notably components of the EGFR and insulin-like growth factor receptor (IGF-1R) pathways - in estrogen-responsive and -dependent human breast cancer cell lines.41^48 In the latter instance, the IGF-1R has also been shown to be activated by estrogen, subsequently recruiting downstream signaling components, notably including insulin receptor substrate-1 (IRS-1), which in turn may be estro-genregulated.46,49 Such actions, which are often antagonized by antiestrogens, could significantly supplement the cellular growth responses directly primed by estrogens.44,45,48

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