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
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