(Thyroid) Hormonal regulation of breast cancer cells

Aleck Hercbergs, Hung Yun Lin, Shaker A. Mousa, Paul J. Davis

Research output: Contribution to journalShort surveypeer-review


Thyroid hormone as L-thyroxine (T4) acts nongenomically at physiological concentrations at its cancer cell surface receptor on integrin αvβ3 (‘thyrointegrin’) to cause cancer cell proliferation. In the case of estrogen receptor (ERα)-positive breast cancer cells, T4 via the integrin promotes ERα-dependent cancer growth in the absence of estrogen. Thus, tumor growth in the post-menopausal patient with ERα-positive cancer may again be ER-dependent because of T4. Additional mechanisms by which T4 may contribute uniquely to aggressive breast cancer behavior—independently of ER—are stimulation of immune checkpoint inhibitor gene expression and of several anti-apoptosis mechanisms. These observations may call for consideration of elimination of host T4 production in breast cancer patients whose response is suboptimal to standard chemotherapy regimens. Euthyroidism in such a setting may be maintained with exogenous 3,3’,5-triiodo-L-thyronine (T3).

Original languageEnglish
Article number1109555
JournalFrontiers in Endocrinology
Publication statusPublished - Jan 2023


  • 3
  • 3’-triiodo-L-thyronine(T3)
  • 5
  • breast cancer
  • estrogen receptor-α (ERα)
  • euthyroid hypothyroxinemia
  • integrin αvβ3
  • L-thyroxine (T4)

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism


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