What is it about?
The bioavailability of IGF-I is controlled by the binding protein, IGF binding protein-3 (IGFBP-3). In addition, IGFBP-3 is a strong anti-proliferative protein that provokes apoptosis and inhibits cell proliferation in prostate cancer. We conducted this study to investigate the association between IGFBP-3 gene polymorphism and serum levels of IGF-I and IGFBP-3 and the incidence of prostate cancer (PCa) and benign prostatic hyperplasia (BPH).
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Why is it important?
With lifetime risk of 17%, prostate cancer (PCa) is the second most common cancer in men, and its incidence is still increasing.. Its molecular pathogenesis is being unraveled, and there is emerging evidence that polymorphic genes may modulate effects of endogenous androgens or environmental toxicants on PCa risk. Insulin like growth factor I (IGF-I) is secreted mainly by the liver. It modulates growth and development, and promotes cellular proliferation, survival and differentiation. In addition to stimulating cell proliferation, IGFs also inhibit the cellular apoptotic properties, thereby facilitating the cell growth. The effects of IGFs on cell proliferation and apoptosis are mediated via a specific cell membrane receptor, insulin-like growth factor-I receptor (IGF-IR). The interactions between IGFs and IGF-IRs are regulated by one of six binding proteins. Among this family, the most abundant binding protein in human serum is IGFBP-3.
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This page is a summary of: Relationship of insulin-like growth factor (IGF) binding protein-3 (IGFBP-3) gene polymorphism with the susceptibility to development of prostate cancer and influence on serum levels of IGF-I, and IGFBP-3, Growth Hormone & IGF Research, June 2011, Elsevier, DOI: 10.1016/j.ghir.2011.03.008.
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