ERK/MAPK regulation of the androgen responsiveness of breast cancer cells

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Diana G Azzam1, Jasmine W T Tay, Melissa A Greeve

  • 1Department of Pathology, Royal Perth Hospital, Perth, Western Australia.

Advances in Experimental Medicine and Biology
|May 24, 2008
PubMed

Insights

Androgen receptor (AR) signaling remains functional in breast cancer cells with hyperactivated ERK/MAPK pathways. These cells maintain AR levels and respond to androgen

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Androgen receptor (AR) is prevalent in breast cancers.
  • Androgens inhibit breast cancer cell proliferation.
  • ERK/MAPK pathway hyperactivity can affect steroid hormone receptor signaling.

Purpose of the Study:

  • To investigate the impact of ERK/MAPK pathway hyperactivity on AR levels and function in breast cancer cells.
  • To determine if breast cancer cells with hyperactivated ERK/MAPK remain sensitive to androgen treatment.

Main Methods:

  • MCF-7 breast cancer cells were engineered to express a constitutively active MEK1 protein (MCF-7-DeltaMEK1).
  • Cells were treated with androgens to assess AR protein levels and proliferation.
  • Cell cycle progression was analyzed using flow cytometry.

Main Results:

  • Androgen treatment of MCF-7-DeltaMEK1 cells induced a transient increase in AR protein levels.
  • Androgens inhibited MCF-7-DeltaMEK1 cell proliferation by 50-60% over 8 days.
  • Androgen treatment led to G1 phase cell cycle accumulation.

Conclusions:

  • ERK/MAPK hyperactivation does not compromise AR levels or androgen sensitivity in breast cancer cells.
  • Breast cancer cells with hyperactivated ERK/MAPK pathways remain susceptible to the growth-inhibitory effects of androgens.
  • This suggests a potential therapeutic window for androgen-based treatments in specific breast cancer subtypes.

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