Abstract
Peroxisome proliferator-activated receptor-delta (PPAR-delta; also known as PPAR-beta) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-delta in colon carcinogenesis using PPAR-delta-deficient (Ppard(-/-)) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-delta. In contrast to previous reports suggesting that activation of PPAR-delta potentiates colon polyp formation, here we show that PPAR-delta attenuates colon carcinogenesis.
Publication types
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Animals
-
Azoxymethane / toxicity
-
Colonic Neoplasms / etiology
-
Colonic Neoplasms / genetics
-
Colonic Neoplasms / prevention & control*
-
Colonic Polyps / etiology
-
Colonic Polyps / genetics
-
Colonic Polyps / pathology
-
Colonic Polyps / prevention & control
-
Disease Models, Animal
-
Mice
-
Mice, Knockout
-
Mice, Mutant Strains
-
Phenotype
-
Receptors, Cytoplasmic and Nuclear / deficiency
-
Receptors, Cytoplasmic and Nuclear / genetics
-
Receptors, Cytoplasmic and Nuclear / physiology*
-
Transcription Factors / deficiency
-
Transcription Factors / genetics
-
Transcription Factors / physiology*
Substances
-
Receptors, Cytoplasmic and Nuclear
-
Transcription Factors
-
Azoxymethane