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The Role of PPARs in Cancer

Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that belong to the nuclear hormone receptor superfamily. PPARα is mainly expressed in the liver, where it activates fatty acid catabolism. PPARα activators have been used to treat dyslipidemia, causing a r...

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Detalles Bibliográficos
Autores principales: Tachibana, Keisuke, Yamasaki, Daisuke, Ishimoto, Kenji, Doi, Takefumi
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2435221/
https://www.ncbi.nlm.nih.gov/pubmed/18584037
http://dx.doi.org/10.1155/2008/102737
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author Tachibana, Keisuke
Yamasaki, Daisuke
Ishimoto, Kenji
Doi, Takefumi
author_facet Tachibana, Keisuke
Yamasaki, Daisuke
Ishimoto, Kenji
Doi, Takefumi
author_sort Tachibana, Keisuke
collection PubMed
description Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that belong to the nuclear hormone receptor superfamily. PPARα is mainly expressed in the liver, where it activates fatty acid catabolism. PPARα activators have been used to treat dyslipidemia, causing a reduction in plasma triglyceride and elevation of high-density lipoprotein cholesterol. PPARδ is expressed ubiquitously and is implicated in fatty acid oxidation and keratinocyte differentiation. PPARδ activators have been proposed for the treatment of metabolic disease. PPARγ2 is expressed exclusively in adipose tissue and plays a pivotal role in adipocyte differentiation. PPARγ is involved in glucose metabolism through the improvement of insulin sensitivity and represents a potential therapeutic target of type 2 diabetes. Thus PPARs are molecular targets for the development of drugs treating metabolic syndrome. However, PPARs also play a role in the regulation of cancer cell growth. Here, we review the function of PPARs in tumor growth.
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spelling pubmed-24352212008-06-26 The Role of PPARs in Cancer Tachibana, Keisuke Yamasaki, Daisuke Ishimoto, Kenji Doi, Takefumi PPAR Res Review Article Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that belong to the nuclear hormone receptor superfamily. PPARα is mainly expressed in the liver, where it activates fatty acid catabolism. PPARα activators have been used to treat dyslipidemia, causing a reduction in plasma triglyceride and elevation of high-density lipoprotein cholesterol. PPARδ is expressed ubiquitously and is implicated in fatty acid oxidation and keratinocyte differentiation. PPARδ activators have been proposed for the treatment of metabolic disease. PPARγ2 is expressed exclusively in adipose tissue and plays a pivotal role in adipocyte differentiation. PPARγ is involved in glucose metabolism through the improvement of insulin sensitivity and represents a potential therapeutic target of type 2 diabetes. Thus PPARs are molecular targets for the development of drugs treating metabolic syndrome. However, PPARs also play a role in the regulation of cancer cell growth. Here, we review the function of PPARs in tumor growth. Hindawi Publishing Corporation 2008 2008-06-18 /pmc/articles/PMC2435221/ /pubmed/18584037 http://dx.doi.org/10.1155/2008/102737 Text en Copyright © 2008 Keisuke Tachibana et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Tachibana, Keisuke
Yamasaki, Daisuke
Ishimoto, Kenji
Doi, Takefumi
The Role of PPARs in Cancer
title The Role of PPARs in Cancer
title_full The Role of PPARs in Cancer
title_fullStr The Role of PPARs in Cancer
title_full_unstemmed The Role of PPARs in Cancer
title_short The Role of PPARs in Cancer
title_sort role of ppars in cancer
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2435221/
https://www.ncbi.nlm.nih.gov/pubmed/18584037
http://dx.doi.org/10.1155/2008/102737
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