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

Ben Ho Park; Bert Vogelstein; Kenneth W. Kinzler

doi:10.1073/pnas.051630998

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

Ben Ho Park, Bert Vogelstein, Kenneth W. Kinzler

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Abstract

Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that have been implicated in a variety of biologic processes. The PPARδ isotype was recently proposed as a downstream target of the adenomatous polyposis coli (APC)/β-catenin pathway in colorectal carcinogenesis. To evaluate its role in tumorigenesis, a PPARδ null cell line was created by targeted homologous recombination. When inoculated as xenografts in nude mice, PPARδ -/- cells exhibited a decreased ability to form tumors compared with PPARδ +/- and wild-type controls. These data suggest that suppression of PPARδ expression contributes to the growth-inhibitory effects of the APC tumor suppressor.

Original language	English (US)
Pages (from-to)	2598-2603
Number of pages	6
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	98
Issue number	5
DOIs	https://doi.org/10.1073/pnas.051630998
State	Published - Feb 27 2001

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abstract = "Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that have been implicated in a variety of biologic processes. The PPARδ isotype was recently proposed as a downstream target of the adenomatous polyposis coli (APC)/β-catenin pathway in colorectal carcinogenesis. To evaluate its role in tumorigenesis, a PPARδ null cell line was created by targeted homologous recombination. When inoculated as xenografts in nude mice, PPARδ -/- cells exhibited a decreased ability to form tumors compared with PPARδ +/- and wild-type controls. These data suggest that suppression of PPARδ expression contributes to the growth-inhibitory effects of the APC tumor suppressor.",

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AB - Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that have been implicated in a variety of biologic processes. The PPARδ isotype was recently proposed as a downstream target of the adenomatous polyposis coli (APC)/β-catenin pathway in colorectal carcinogenesis. To evaluate its role in tumorigenesis, a PPARδ null cell line was created by targeted homologous recombination. When inoculated as xenografts in nude mice, PPARδ -/- cells exhibited a decreased ability to form tumors compared with PPARδ +/- and wild-type controls. These data suggest that suppression of PPARδ expression contributes to the growth-inhibitory effects of the APC tumor suppressor.

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

Abstract

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