Insulin-like growth factor-I and estrogen interactions in breast cancer.
There is increasing evidence that estradiol and insulin-like growth factor-I (IGF-I) act through a complex cross-talk mechanism to stimulate the proliferation of normal mammary epithelium to increase the risk of breast cancer. The emerging model of cross-talk suggests that estradiol regulates the expression of IGF-I and the IGF receptor I. The subsequent binding of IGF-I to its receptor initiates an intracellular signal transduction pathway that activates transcription factors, including the estrogen receptor. Recent studies show that the effects of IGF-I on estrogen receptor activity are mediated in part by the protein kinase A and phosphatidylinositol-3-kinase/Akt pathways.
Martin
Mary Beth
MB
Department of Oncology, Vincent T. Lombardi Cancer Center, Georgetown University, Washington, DC, USA. martinmb@georgetown.edu
Stoica
Adriana
A
D001940:Breast / Q000166:cytology; D001943:Breast Neoplasms / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology*; D002455:Cell Division / Q000502:physiology; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D004847:Epithelial Cells / Q000166:cytology; D004967:Estrogens / Q000502:physiology*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000502:physiology*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism
D004967:Estrogens; D007334:Insulin-Like Growth Factor I; D019869:Phosphatidylinositol 3-Kinases; D017868:Cyclic AMP-Dependent Protein Kinases