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Activation of the human FP prostanoid receptor disrupts mitosis progression and generates aneuploidy and polyploidy

X-B Chen1, J W Regan

  • 1Department of Pharmacology and Toxicology, College of Pharmacy, The University of Arizona, Tucson, Arizona 85721-0207, USA.

Cellular and Molecular Life Sciences : CMLS
|December 27, 2005
PubMed

Insights

Prostaglandin F(2alpha) (PGF(2alpha)) delays mitosis and causes genomic instability by interfering with nuclear division via Rho signaling. This may explain its tumor-promoting effects in skin carcinogenesis.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Prostaglandin F(2alpha) (PGF(2alpha)) is an endogenous tumor promoter in skin carcinogenesis models.
  • The precise mechanisms by which PGF(2alpha) influences cell cycle progression are not fully understood.

Purpose of the Study:

  • To investigate the effects of PGF(2alpha) on cell cycle events in HEK cells expressing the human FP receptor.
  • To elucidate the molecular pathways involved in PGF(2alpha)-mediated cell cycle disruption.

Main Methods:

  • Cell cycle analysis of HEK cells treated with PGF(2alpha).
  • Assessment of cyclin B1 expression and Cdc2 kinase activity.
  • Microscopic observation of spindle formation and chromosome alignment.
  • Evaluation of cytokinesis and ploidy.
  • Analysis of Rho signaling pathway involvement using dominant-negative Rho.

Main Results:

  • PGF(2alpha) treatment delayed mitosis and increased cyclin B1 expression and Cdc2 kinase activity.
  • Observed were multipolar spindles, misaligned chromosomes, and defective cytokinesis, leading to aneuploidy and polyploidy.
  • Inhibition of Rho signaling attenuated PGF(2alpha)-induced cell cycle delay and prevented micronuclei formation.

Conclusions:

  • PGF(2alpha) activates Rho signaling through the FP receptor, interfering with nuclear division.
  • The resulting aneuploidy and genomic instability may contribute to the tumor-promoting properties of PGF(2alpha).

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