Harman Fred S, Nicol Christopher J, Marin Holly E, Ward Jerrold M, Gonzalez Frank J, Peters Jeffrey M
Department of Veterinary Science and The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802, USA.
Nat Med. 2004 May;10(5):481-3. doi: 10.1038/nm1026. Epub 2004 Mar 28.
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.
过氧化物酶体增殖物激活受体δ（PPAR-δ；也称为PPAR-β）在结肠肿瘤中高表达，但其对结肠癌的作用尚不清楚。我们使用PPAR-δ缺陷（Ppard(-/-)）小鼠研究了PPAR-δ在结肠癌发生中的作用。在Min突变体和化学诱导的小鼠模型中，PPAR-δ纯合缺失的小鼠结肠息肉形成明显更多。与之前报道的PPAR-δ激活会增强结肠息肉形成相反，我们在此表明PPAR-δ可减弱结肠癌发生。
