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Progestin and G protein-coupled receptor 30 inhibit mitogen-activated protein kinase activity in MCF-7 breast cancer

Tytti M Ahola1, Niina Alkio, Tommi Manninen

  • 1Department of Cell Biology, Medical School, University of Tampere, 33014 Tampere, Finland. ta55935@uta.fi

Endocrinology
|November 26, 2002
PubMed

Insights

Progestin and G protein-coupled receptor (GPR)30 inhibit MAPK activity, leading to growth inhibition in MCF-7 cells. This study reveals progestin-induced ERK inactivation is mediated through GPR30.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Signaling

Background:

  • G protein-coupled receptor (GPR)30 is crucial for progestin-induced growth inhibition.
  • Signal transduction pathways mediating progestin signaling require further elucidation.

Purpose of the Study:

  • To investigate the signal transduction pathways involved in progestin-mediated signaling.
  • To determine the role of GPR30 in progestin-induced growth inhibition and MAPK pathway regulation.

Main Methods:

  • MCF-7 cells were treated with progestin, medroxyprogesterone acetate (MPA), and MAPK kinase inhibitors (PD98059, U0126).
  • ERK-1 and -2 activities were assessed using immunoblotting and kinase assays.
  • GPR30 expression was manipulated using transient expression and antisense techniques.

Main Results:

  • Progestin did not enhance the growth inhibitory effect of MAPK kinase inhibitors.
  • MPA induced a late decrease in ERK-1 and -2 activities, which was abrogated by antiprogestin.
  • GPR30 expression decreased ERK activity, while GPR30 knockdown increased ERK activity and conferred resistance to MAPK inhibitors.
  • MPA-induced ERK inactivation was blocked by GPR30 antisense.

Conclusions:

  • Progestin and GPR30 inhibit MAPK activity, suggesting a role in growth inhibition.
  • Progestin-induced ERK inactivation is mediated through GPR30.
  • Up-regulation of GPR30 by progestin leads to ERK inactivation and growth inhibition in MCF-7 cells.

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