Peroxisome proliferator–activated receptor-δ attenuates colon carcinogenesis

被引:0
|
作者
Fred S Harman
Christopher J Nicol
Holly E Marin
Jerrold M Ward
Frank J Gonzalez
Jeffrey M Peters
机构
[1] The Pennsylvania State University,Department of Veterinary Science and The Center for Molecular Toxicology and Carcinogenesis
[2] University Park,undefined
[3] Graduate Program in Biochemistry,undefined
[4] Microbiology,undefined
[5] and Molecular Biology,undefined
[6] The Pennsylvania State University,undefined
[7] University Park,undefined
[8] Laboratory of Metabolism,undefined
[9] National Cancer Institute,undefined
[10] Veterinary and Tumor Pathology Section,undefined
[11] Office of Laboratory Animal Resources,undefined
[12] National Cancer Institute,undefined
来源
Nature Medicine | 2004年 / 10卷
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摘要
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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页码:481 / 483
页数:2
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