Role of insulin-like growth factors in steroid modulated proliferation

J Steroid Biochem Mol Biol. 1994 Oct;51(1-2):1-9. doi: 10.1016/0960-0760(94)90109-0.


The mechanism by which steroids influence cell proliferation is poorly understood although an understanding of this process might facilitate the development of strategies to modulate the tissue-specific activity of steroid hormones. In this article, the evidence that steroid hormones interact with the insulin-like growth factor (IGF) signal transduction pathway is reviewed for three different tissues. In osteoblasts, oestradiol stimulates the production of IGF-I which appears to act as an autocrine growth factor. In uterine tissue, oestradiol increases the synthesis of IGF-I in the stroma which then modulates the proliferation of epithelial cells although there is also evidence that oestradiol can modulate the sensitivity of uterine epithelial cells to IGFs. In breast cancer, oestrogens may increase IGF-II synthesis in epithelial cells, increase the sensitivity of breast cancer cells to IGFs (possibly by modulating type I IGF receptor levels) as well as resulting components of the IGF signal transduction pathway resulting in induction of immediate early genes. There therefore appears to be a variety of ways in which oestradiol interact with the IGF signal transduction pathway and these may be applicable to other malignant and normal tissues and other groups of steroid hormones.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Division / drug effects*
  • Humans
  • Neoplasms / pathology
  • Signal Transduction / drug effects
  • Somatomedins / physiology*
  • Steroids / pharmacology*


  • Somatomedins
  • Steroids