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Anti-oestrogens induce the secretion of active transforming growth factor beta from human fetal fibroblasts

A A Colletta1, L M Wakefield, F V Howell

  • 1Department of Surgery, Kings College School of Medicine and Dentistry, Rayne Institute, London, UK.

British Journal of Cancer
|September 1, 1990
PubMed

Insights

Anti-oestrogens may treat breast cancer by stimulating stromal cells to produce growth-inhibiting transforming growth factor beta (TGF-beta), independent of tumour oestrogen receptors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Anti-oestrogen therapy is standard for oestrogen receptor-positive breast cancer.
  • Clinical response to adjuvant anti-oestrogens is independent of primary tumour oestrogen receptor (ER) levels.
  • A novel mechanism for anti-oestrogen action is needed to explain this observation.

Purpose of the Study:

  • To investigate if human stromal cells can increase synthesis of transforming growth factor beta (TGF-beta) in response to anti-oestrogens.
  • To explore a potential ER-independent mechanism of anti-oestrogen action in breast cancer.

Main Methods:

  • Two human fetal fibroblast strains were used as models for breast cancer stromal fibroblasts.
  • Cells were treated with anti-oestrogens.
  • TGF-beta synthesis was measured.
  • Oestrogen receptor (ER) and ER mRNA were assessed using ligand binding, immunoassay, and Northern analysis.

Main Results:

  • Human fetal fibroblast strains significantly increased synthesis of biologically active TGF-beta upon addition of anti-oestrogens.
  • No oestrogen receptor (ER) or ER mRNA was detected in either fibroblast strain.
  • This suggests an ER-independent response.

Conclusions:

  • Human stromal cells can respond to anti-oestrogens by increasing TGF-beta synthesis.
  • This provides a potential ER-independent mechanism for anti-oestrogen therapy in breast cancer.
  • This may explain the efficacy of anti-oestrogens even in ER-negative tumours.

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