MCF-7 cell apoptosis and cell cycle arrest: non-genomic effects of progesterone and mifepristone (RU-486)

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Renathe Fjelldal1, Bjørn T Moe, Anne Ørbo

  • 1Medical Pharmacology and Toxicology Research Unit, Department of Medical Biology, Faculty of Health Sciences, University of Tromsø, N-9037 Tromsø, Norway.

Anticancer Research
|December 29, 2010
PubMed
Abstract

Insights

Progesterone and mifepristone exhibit non-genomic effects, inhibiting cancer cell growth through cell cycle arrest and apoptosis. These findings highlight the antiproliferative potential of non-genomic progestin actions.

Area of Science:

  • Pharmacology
  • Cell Biology
  • Cancer Research

Background:

  • Progestins act through nuclear receptors (nPR) and non-genomic pathways (mPR, enzymes, etc.).
  • Non-genomic progestin effects are increasingly recognized for their role in cell growth regulation.

Purpose of the Study:

  • To differentiate and characterize nPR-initiated (genomic) and non-genomic effects of progestins.
  • To investigate the antiproliferative and cytotoxic mechanisms of progesterone (PG) and mifepristone (MF) in cancer cell lines.

Main Methods:

  • Exposure of nPR-positive (MCF-7) and nPR-negative (C4-I) cell lines to PG and MF for 96 hours.
  • Daily monitoring of cell count, cell cycle analysis, and apoptosis assays.

Main Results:

  • Progesterone (PG) demonstrated nPR-initiated growth stimulation below 1 μM in MCF-7 cells, blocked by mifepristone (MF).
  • Both PG and MF exhibited concentration-dependent growth inhibition (antiproliferative effects) between 1 μM and 100 μM, mediated by non-genomic actions.
  • MF showed equal or greater potency than PG in reducing cell density (IC50 values ranging from 5.3 to 12.8 μM).
  • Growth inhibition resulted from cell cycle arrest and apoptosis; combined PG and MF showed potentiated effects.

Conclusions:

  • The antiproliferative/cytotoxic effects of PG and MF at concentrations between 1 and 100 μM are primarily non-genomic.
  • Non-genomic progestin actions play a significant role in inhibiting cancer cell proliferation.

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