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¹ Department of Veterinary Physiology and Pharmacology,
² Department of Veterinary Anatomy and Public Health,
³ Department of Veterinary Pathobiology, Texas A&M University, College Station, TX 77843, USA
⁴ Institute of Biosciences and Technology, Texas A&M University System Health Science Center, 2121 West Holcombe Boulevard, Houston, TX 77030, USA

(Requests for offprints should be addressed to S H Safe, Department of Veterinary Physiology & Pharmacology, Texas A&M University, 4466 TAMU, College Station, TX 77843-4466, USA; Email: ssafe{at}cvm.tamu.edu)

Insulin-like growth factor-I (IGF-I) is a mitogenic polypeptide that induces proliferation of MCF-7 breast cancer cells, and cotreatment with the phosphoinositide 3-kinase (PI3-K) inhibitor LY294002 and the antiestrogen ICI 182780 inhibits IGF-I-induced growth. The role of estrogen receptor (ER) in mediating responses induced by IGF-I was investigated in cells transfected with small inhibitory RNA for ER (iER). The results showed that IGF-I-dependent phosphorylation of Akt and mitogen-activated protein kinase, induction of G₁–S-phase progression and enhanced expression of cyclin D1 and cyclin E were dependent on ER. Moreover, these same IGF-I-induced responses were also inhibited by the antiestrogen ICI 182780 and this was in contrast to a previous report suggesting that ICI 182780 did not affect IGF-I-dependent activation of PI3-K or induction of cyclin D1 expression. ICI 182780 exhibits antimitogenic activity and iER inhibits G₁–S-phase progression and proliferation of MCF-7 cells treated with IGF-I, suggesting that the effects of the antiestrogen are primarily related to downregulation of ER.

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