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Peroxisome Proliferator-Activated Receptors and Progression of Colorectal Cancer

The peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily. These receptors are also ligand-dependent transcription factors responsible for the regulation of cellular events that range from glucose and lipid homeostases to cell differentiation and...

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Detalles Bibliográficos
Autores principales: Wang, Dingzhi, DuBois, Raymond N.
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2422873/
https://www.ncbi.nlm.nih.gov/pubmed/18551185
http://dx.doi.org/10.1155/2008/931074
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author Wang, Dingzhi
DuBois, Raymond N.
author_facet Wang, Dingzhi
DuBois, Raymond N.
author_sort Wang, Dingzhi
collection PubMed
description The peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily. These receptors are also ligand-dependent transcription factors responsible for the regulation of cellular events that range from glucose and lipid homeostases to cell differentiation and apoptosis. The importance of these receptors in lipid homeostasis and energy balance is well established. In addition to these metabolic and anti-inflammatory properties, emerging evidence indicates that PPARs can function as either tumor suppressors or accelerators, suggesting that these receptors are potential candidates as drug targets for cancer prevention and treatment. However, conflicting results have emerged regarding the role of PPARs on colon carcinogenesis. Therefore, further investigation is warranted prior to considering modulation of PPARs as an efficacious therapy for colorectal cancer chemoprevention and treatment.
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spelling pubmed-24228732008-06-12 Peroxisome Proliferator-Activated Receptors and Progression of Colorectal Cancer Wang, Dingzhi DuBois, Raymond N. PPAR Res Review Article The peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily. These receptors are also ligand-dependent transcription factors responsible for the regulation of cellular events that range from glucose and lipid homeostases to cell differentiation and apoptosis. The importance of these receptors in lipid homeostasis and energy balance is well established. In addition to these metabolic and anti-inflammatory properties, emerging evidence indicates that PPARs can function as either tumor suppressors or accelerators, suggesting that these receptors are potential candidates as drug targets for cancer prevention and treatment. However, conflicting results have emerged regarding the role of PPARs on colon carcinogenesis. Therefore, further investigation is warranted prior to considering modulation of PPARs as an efficacious therapy for colorectal cancer chemoprevention and treatment. Hindawi Publishing Corporation 2008 2008-06-05 /pmc/articles/PMC2422873/ /pubmed/18551185 http://dx.doi.org/10.1155/2008/931074 Text en Copyright © 2008 D.Wang and Raymond N. DuBois. 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
Wang, Dingzhi
DuBois, Raymond N.
Peroxisome Proliferator-Activated Receptors and Progression of Colorectal Cancer
title Peroxisome Proliferator-Activated Receptors and Progression of Colorectal Cancer
title_full Peroxisome Proliferator-Activated Receptors and Progression of Colorectal Cancer
title_fullStr Peroxisome Proliferator-Activated Receptors and Progression of Colorectal Cancer
title_full_unstemmed Peroxisome Proliferator-Activated Receptors and Progression of Colorectal Cancer
title_short Peroxisome Proliferator-Activated Receptors and Progression of Colorectal Cancer
title_sort peroxisome proliferator-activated receptors and progression of colorectal cancer
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2422873/
https://www.ncbi.nlm.nih.gov/pubmed/18551185
http://dx.doi.org/10.1155/2008/931074
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