Progesterone inhibits human breast cancer cell growth through transcriptional upregulation of the cyclin-dependent kinase inhibitor p27Kip1 gene

FEBS Lett. 2005 Oct 24;579(25):5535-41. doi: 10.1016/j.febslet.2005.08.084. Epub 2005 Sep 27.

Abstract

The effects of progesterone derivatives on breast cancer development are still controversial, probably accounting for their biphasic, opposed effects on mammary cell-cycle regulation. Here, we demonstrate in vitro that the growth-inhibitory effects of progesterone on breast cancer T-47D cells require the transcriptional upregulation of the cyclin-dependent kinase inhibitor p27(Kip1) (p27) gene. A statistical analysis of human tumor biopsies further indicates that p27 mRNA levels correlate to progesterone receptor (PR) levels. Moreover, p27 gene expression is inversely associated with tumor aggressiveness, and is a prognostic factor of favorable disease outcome. Thus, progesterone derivatives selectively activating the p27 gene promoter could be promising drugs against breast cancer progression.

MeSH terms

  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / genetics
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cyclin-Dependent Kinase Inhibitor p27 / biosynthesis
  • Cyclin-Dependent Kinase Inhibitor p27 / genetics*
  • Humans
  • Intracellular Signaling Peptides and Proteins / genetics*
  • Progesterone / pharmacology
  • Progesterone / therapeutic use*
  • Promoter Regions, Genetic
  • Receptors, Progesterone / metabolism*
  • Sp1 Transcription Factor / metabolism
  • Transcription, Genetic / drug effects*
  • Up-Regulation

Substances

  • CDKN1B protein, human
  • Intracellular Signaling Peptides and Proteins
  • Receptors, Progesterone
  • Sp1 Transcription Factor
  • Cyclin-Dependent Kinase Inhibitor p27
  • Progesterone