Efavirenz directly modulates the oestrogen receptor and induces breast cancer cell growth

M. J. Sikora, J. M. Rae, M. D. Johnson, Z. Desta

Research output: Contribution to journalArticle

20 Scopus citations


Objectives: Efavirenz-based HIV therapy is associated with breast hypertrophy and gynaecomastia. Here, we tested the hypothesis that efavirenz induces gynaecomastia through direct binding and modulation of the oestrogen receptor (ER). Methods: To determine the effect of efavirenz on growth, the oestrogen-dependent, ER-positive breast cancer cell lines MCF-7, T47D and ZR-75-1 were treated with efavirenz under oestrogen-free conditions in the presence or absence of the anti-oestrogen ICI 182,780. Cells treated with 17β-oestradiol in the absence or presence of ICI 182,780 served as positive and negative controls, respectively. Cellular growth was assayed using the crystal violet staining method and an in vitro receptor binding assay was used to measure the ER binding affinity of efavirenz. Results: Efavirenz induced growth in MCF-7 cells with an estimated effective concentration for half-maximal growth (EC50) of 15.7 μM. This growth was reversed by ICI 182,780. Further, efavirenz binds directly to the ER [inhibitory concentration for half maximal binding (IC50) of ∼52 μM] at a roughly 1000-fold higher concentration than observed with 17β-oestradiol. Conclusions: Our data suggest that efavirenz-induced gynaecomastia may be caused, at least in part, by drug-induced ER activation in breast tissues.

Original languageEnglish (US)
Pages (from-to)603-607
Number of pages5
JournalHIV Medicine
Issue number9
StatePublished - Oct 1 2010


  • Efavirenz
  • Gynaecomastia
  • Highly active antiretroviral therapy
  • Oestrogen receptor
  • Oestrogens

ASJC Scopus subject areas

  • Infectious Diseases
  • Pharmacology (medical)
  • Health Policy

Fingerprint Dive into the research topics of 'Efavirenz directly modulates the oestrogen receptor and induces breast cancer cell growth'. Together they form a unique fingerprint.

  • Cite this