Loma Linda University

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Willie Davis, PhD
Chair, Pharmaceutical and Administrative Sciences
School of Pharmacy
Associate Professor, Pharmaceutical and Administrative Sciences
School of Pharmacy
Associate Professor, Basic Sciences
School of Medicine
Member, Pharmaceutical Science, SP, Faculty of Graduate Studies
Publications    Scholarly Journals--Published
  •  “Insulin-like Growth Factor-2(IGF-2) Activates Estrogen Receptor-alpha and –beta Via the IGF-1 and the Insulin Receptors in Breast Cancer Cells.” A Richardson, N. Hamilton, W. Davis, C. Brito and D. Deleon.  Growth Factors, April – June 2011; 29(2-3): 1 – 12. ( 4/2011 ) Link...
     The estrogen receptor (ER) is a primary target for breast cancer (BC) treatment. As BC progresses to estrogen-independent growth, the insulin-like growth factor-1 receptor (IGF-1R) and the ER interact in synergistic cross-talk mechanisms, which result in enhanced activation of both receptors'''' signaling cascades. Insulin-like growth factor-2 (IGF-2) is critical in BC progression and its actions are mediated by the IGF-1R. Our previous studies showed that IGF-2 regulates survival genes that protect the mitochondria and promote chemoresistance. In this study, we analyzed BC cells by subcellular fractionation, Western-Blot, qRT-PCR, and siRNA analysis. Our results demonstrate that IGF-2 activates ER-α and ER-β, and modulates their translocation to the nucleus, membrane organelles, and the mitochondria. IGF-2 actions are mediated by the IGF-1R and the insulin receptor. This novel mechanism of IGF-2 synergistic cross-talk signaling with ER-α and ER-β can promote estrogen-independent BC progression and provide new therapeutic targets for the treatment of BC patients. http://www.ncbi.nlm.nih.gov/pubmed/21410323