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Peroxisome proliferator–activated receptor-δ attenuates colon carcinogenesis


Peroxisome proliferator–activated receptor-δ (PPAR-δ; also known as PPAR-β) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-δ in colon carcinogenesis using PPAR-δ-deficient (Ppard−/− ) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-δ. In contrast to previous reports suggesting that activation of PPAR-δ potentiates colon polyp formation, here we show that PPAR-δ attenuates colon carcinogenesis.

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Figure 1: Phenotypes of Apc+/minPpard+/+ and Apc+/minPpard−/− mice.

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Animal care and procedures were approved by the Institutional Animal Care and Use Committees at The Pennsylvania State University and National Cancer Institute. The authors thank A. Burns and R. Horner for technical assistance, and G. Perdew and A. Kusnadi for providing the COS-1 cell lysate. This work was supported by National Cancer Institute grants CA97999 and CA89607 (J.M.P.).

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Correspondence to Jeffrey M Peters.

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The authors declare no competing financial interests.

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Harman, F., Nicol, C., Marin, H. et al. Peroxisome proliferator–activated receptor-δ attenuates colon carcinogenesis. Nat Med 10, 481–483 (2004).

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