The estrogen receptor-alpha (ER-α) is a Type I nuclear receptor that is over-expressed in the majority of human breast cancers and plays a significant role in the development and progression of these cancers. As estrogen plays important roles in the etiology of breast cancer and the growth of established ER-α expressing cancers, intense interest has been generated in understanding the mechanisms by which ER-α signaling is regulated physiologically and using this knowledge to develop interventions to inhibit ER-α signaling. These efforts have met with some success in the development of pharmacologic agents that can reduce breast cancer risk, prevent recurrence of established cancers, and treat advanced cancers with considerably less side effects than cytotoxic chemotherapy. Here, we will review some of the mechanisms that operate to inhibit ER-α signaling and describe how pharmacologic agents and dietary factors interact with ER-α to block its activity. In the process of reviewing these mechanisms, we will highlight their clinical implications.

Numerous studies suggest that loss of E-cadherin is necessary to induce Epithelial–mesenchymal transition (EMT) and metastasis. Snail is a major contributor to EMTs. The Snail family of zinc-finger transcription factors interact with the E-cadherin promoter to repress transcription during EMT. The present article reviews the regulation of E-cadherin and discusses recent novel insights into the molecular basis in the process of EMT.