Peroxisome proliferator-activated receptor gamma induces pancreatic cancer cell apoptosis

Biochem Biophys Res Commun. 2001 Sep 21;287(2):522-9. doi: 10.1006/bbrc.2001.5619.


Peroxisome proliferator-activated receptor gamma (PPAR-gamma) decreases the growth of certain cancer cells. In the present study, we found that six different human pancreatic cancer cell lines (AsPC-1, BxPC-3, Capan-2, HPAF-II, MIA PaCa-2, and PANC-1) expressed PPAR-gamma m-RNA and synthesized the protein. The endogenous and exogenous PPAR-gamma ligands 15-deoxy-d12,14-prostaglandin J(2) (15-PGJ(2)) and ciglitazone decreased cell number, cell viability, and increased floating/attached ratio, in a time- and dose-dependent fashion. 15-PGJ(2) increased intracellular nucleosome concentration after 6 h, but did not increase caspase-3 activity even after 96 h. Combined treatment with both 15-PGJ(2) and the caspase-3 inhibitor DEVD-CHO had no effect on cell viability, but the general caspase inhibitor ZVAD-FMK reduced 15-PGJ(2)-induced apoptosis. We concluded that the six human pancreatic cancer cells tested all expressed PPAR-gamma receptor, and treatment with PPAR-gamma agonists decreased cell viability and growth in a time- and dose-dependent manner. These effects were partially mediated by induction of caspase-3 independent apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis*
  • Caspase 3
  • Caspases / metabolism
  • Cell Division / physiology
  • Cell Survival / physiology
  • Humans
  • Pancreatic Neoplasms / pathology*
  • Receptors, Cytoplasmic and Nuclear / biosynthesis
  • Receptors, Cytoplasmic and Nuclear / physiology*
  • Transcription Factors / biosynthesis
  • Transcription Factors / physiology*
  • Tumor Cells, Cultured


  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • CASP3 protein, human
  • Caspase 3
  • Caspases