Roman Jesse
Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA.
J Investig Med. 2008 Feb;56(2):528-33. doi: 10.2310/JIM.0b013e3181659932.
Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptor family of transcriptional modulators. In addition to their known roles in regulation of metabolism and inflammation, PPARs have also been implicated in carcinogenesis based on studies showing their ability to modulate cellular differentiation, proliferation, and apoptosis. Of the 3 PPARs identified to date (PPARalpha, PPARbeta/delta, and PPARgamma), PPARgamma has been studied the most in part because of the availability of PPARgamma agonists (also known as PPARgamma ligands). In many tumor cells, including lung carcinoma cells, activation of PPARgamma results in decreased cellular proliferation; this is particularly true for non-small cell lung carcinoma, the most common malignant lung tumor in the United States. Studies performed in xenograft models of lung cancer also show decreased tumor growth and progression in animals treated with PPARgamma ligands. More recently, data are emerging from retrospective clinical studies that suggest a protective role for PPARgamma ligands on the incidence of lung cancer. This review summarizes the available data that implicate PPARs in lung carcinogenesis while focusing on PPARgamma as a potential target for the development of novel anti-lung cancer treatment strategies.
过氧化物酶体增殖物激活受体(PPARs)是转录调节因子核受体家族的成员。除了在调节代谢和炎症方面的已知作用外,基于显示其调节细胞分化、增殖和凋亡能力的研究,PPARs也与致癌作用有关。在迄今已鉴定出的3种PPARs(PPARα、PPARβ/δ和PPARγ)中,PPARγ的研究最为深入,部分原因是有PPARγ激动剂(也称为PPARγ配体)可用。在许多肿瘤细胞中,包括肺癌细胞,PPARγ的激活会导致细胞增殖减少;对于非小细胞肺癌(美国最常见的恶性肺肿瘤)来说尤其如此。在肺癌异种移植模型中进行的研究还表明,用PPARγ配体治疗的动物肿瘤生长和进展减缓。最近,回顾性临床研究的数据表明,PPARγ配体对肺癌发病率具有保护作用。本综述总结了提示PPARs参与肺癌发生的现有数据,同时将重点放在PPARγ作为开发新型抗肺癌治疗策略的潜在靶点上。