Crosstalk between IGF1R and estrogen receptor signaling in breast cancer

Dedra H. Fagan, Douglas Yee

Research output: Contribution to journalReview articlepeer-review

143 Scopus citations


After the discovery that depriving certain breast tumors of estrogen promoted tumor regression, therapeutic strategies aimed at depriving tumors of this hormone were developed. The tumorigenic properties of estrogen are regulated through the estrogen receptor-α (ER), making understanding the mechanisms that activate this receptor highly relevant. In addition to estrogen activating the ER, other growth factor pathways, such as the insulin-like growth factors (IGFs), can activate the ER. This review will examine the interaction between these two pathways. Estrogen can activate the growth stimulatory properties of the IGF pathway via ER's genomic and non-genomic functions. Further, blockade of ER function can inhibit IGF-mediated mitogenesis and blocking IGF action can inhibit estrogen stimulation of breast cancer cells. Collectively, these observations suggest that the two growth regulatory pathways are tightly linked and a more thorough understanding of the mechanism of this crosstalk could lead to improved therapeutic strategies in breast cancer.

Original languageEnglish (US)
Pages (from-to)423-429
Number of pages7
JournalJournal of mammary gland biology and neoplasia
Issue number4
StatePublished - 2008


  • Breast cancer
  • Estrogen receptor
  • Insulin-like growth factors


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