Genetic disruption of PPARδ decreases the tumorigenicity of human colon cancer cells

被引:217
作者
Park, BH
Vogelstein, B
Kinzler, KW
机构
[1] Johns Hopkins Oncol Ctr, Baltimore, MD 21231 USA
[2] Howard Hughes Med Inst, Baltimore, MD 21231 USA
关键词
D O I
10.1073/pnas.051630998
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that have been implicated in a variety of biologic processes. The PPAR delta isotype was recently proposed as a downstream target of the adenomatous polyposis coli (APC)/beta catenin pathway in colorectal carcinogenesis. To evaluate its role in tumorigenesis, a PPAR delta null cell line was created by targeted homologous recombination. When inoculated as xenografts in nude mice, PPAR delta -/- cells exhibited a decreased ability to form tumors compared with PPAR delta +/- and wild-type controls. These data suggest that suppression of PPAR delta expression contributes to the growth-inhibitory effects of the APC tumor suppressor.
引用
收藏
页码:2598 / 2603
页数:6
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