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PPARγ and PPARδ as Modulators of Neoplasia and Cell Fate
PPARγ and PPARδ agonists represent unique classes of drugs that act through their ability to modulate gene transcription associated with intermediary metabolism, differentiation, tumor suppression, and in some instances proliferation and cell adhesion. PPARγ agonists are used by millions of people e...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2008
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430014/ https://www.ncbi.nlm.nih.gov/pubmed/18566686 http://dx.doi.org/10.1155/2008/247379 |
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author | Glazer, Robert I. Yuan, Hongyan Xie, Zhihui Yin, Yuzhi |
author_facet | Glazer, Robert I. Yuan, Hongyan Xie, Zhihui Yin, Yuzhi |
author_sort | Glazer, Robert I. |
collection | PubMed |
description | PPARγ and PPARδ agonists represent unique classes of drugs that act through their ability to modulate gene transcription associated with intermediary metabolism, differentiation, tumor suppression, and in some instances proliferation and cell adhesion. PPARγ agonists are used by millions of people each year to treat type 2 diabetes but may also find additional utility as relatively nontoxic potentiators of chemotherapy. PPARδ agonists produce complex actions as shown by their tumor promoting effects in rodents and their cholesterol-lowering action in dyslipidemias. There is now emerging evidence that PPARs regulate tumor suppressor genes and developmental pathways associated with transformation and cell fate determination. This review discusses the role of PPARγ and PPARδ agonists as modulators of these processes. |
format | Text |
id | pubmed-2430014 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-24300142008-06-19 PPARγ and PPARδ as Modulators of Neoplasia and Cell Fate Glazer, Robert I. Yuan, Hongyan Xie, Zhihui Yin, Yuzhi PPAR Res Review Article PPARγ and PPARδ agonists represent unique classes of drugs that act through their ability to modulate gene transcription associated with intermediary metabolism, differentiation, tumor suppression, and in some instances proliferation and cell adhesion. PPARγ agonists are used by millions of people each year to treat type 2 diabetes but may also find additional utility as relatively nontoxic potentiators of chemotherapy. PPARδ agonists produce complex actions as shown by their tumor promoting effects in rodents and their cholesterol-lowering action in dyslipidemias. There is now emerging evidence that PPARs regulate tumor suppressor genes and developmental pathways associated with transformation and cell fate determination. This review discusses the role of PPARγ and PPARδ agonists as modulators of these processes. Hindawi Publishing Corporation 2008 2008-06-12 /pmc/articles/PMC2430014/ /pubmed/18566686 http://dx.doi.org/10.1155/2008/247379 Text en Copyright © 2008 Robert I. Glazer 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 Glazer, Robert I. Yuan, Hongyan Xie, Zhihui Yin, Yuzhi PPARγ and PPARδ as Modulators of Neoplasia and Cell Fate |
title | PPARγ and PPARδ as Modulators of Neoplasia and Cell Fate |
title_full | PPARγ and PPARδ as Modulators of Neoplasia and Cell Fate |
title_fullStr | PPARγ and PPARδ as Modulators of Neoplasia and Cell Fate |
title_full_unstemmed | PPARγ and PPARδ as Modulators of Neoplasia and Cell Fate |
title_short | PPARγ and PPARδ as Modulators of Neoplasia and Cell Fate |
title_sort | pparγ and pparδ as modulators of neoplasia and cell fate |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430014/ https://www.ncbi.nlm.nih.gov/pubmed/18566686 http://dx.doi.org/10.1155/2008/247379 |
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