A Role for PPARβ/δ in Tumor Stroma and Tumorigenesis

Peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) is a transcription factor that is activated by endogenous fatty acid ligands and by synthetic agonists. Its role in the regulation of skeletal muscle fatty acid catabolism, glucose homeostasis, and cellular differentiation has been established...

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Main Authors: Rolf Müller, Martin Kömhoff, Jeffrey M. Peters, Sabine Müller-Brüsselbach
Format: Article
Language:English
Published: Wiley 2008-01-01
Series:PPAR Research
Online Access:http://dx.doi.org/10.1155/2008/534294
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author Rolf Müller
Martin Kömhoff
Jeffrey M. Peters
Sabine Müller-Brüsselbach
author_facet Rolf Müller
Martin Kömhoff
Jeffrey M. Peters
Sabine Müller-Brüsselbach
author_sort Rolf Müller
collection DOAJ
description Peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) is a transcription factor that is activated by endogenous fatty acid ligands and by synthetic agonists. Its role in the regulation of skeletal muscle fatty acid catabolism, glucose homeostasis, and cellular differentiation has been established in multiple studies. On the contrary, a role for PPARβ/δ in tumorigenesis is less clear because there are contradictory reports in the literature. However, the majority of these studies have not examined the role of PPARβ/δ in the tumor stroma. Recent evidence suggests that stromal PPARβ/δ regulates tumor endothelial cell proliferation and promotes differentiation leading to the properly orchestrated events required for tumor blood vessel formation. This review briefly summarizes the significance of these studies that may provide clues to help explain the reported discrepancies in the literature regarding the role of PPARβ/δ in tumorigenesis.
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spelling doaj-art-1a0c22c3fed0489690919c2f4584f3912025-02-03T05:44:57ZengWileyPPAR Research1687-47571687-47652008-01-01200810.1155/2008/534294534294A Role for PPARβ/δ in Tumor Stroma and TumorigenesisRolf Müller0Martin Kömhoff1Jeffrey M. Peters2Sabine Müller-Brüsselbach3Institute of Molecular Biology and Tumor Research (IMT), Philipps-University, Emil-Mannkopff-Strasse 2, 35032 Marburg, GermanyDepartment of Pediatrics, Philipps-University, Baldingerstrasse, 35043 Marburg, GermanyDepartment of Veterinary and Biomedical Sciences and Center for Molecular Toxicology and Carcinogenesis, 312 Life Sciences Building, The Pennsylvania State University, University Park, PA 16802-1504, USAInstitute of Molecular Biology and Tumor Research (IMT), Philipps-University, Emil-Mannkopff-Strasse 2, 35032 Marburg, GermanyPeroxisome proliferator-activated receptor-β/δ (PPARβ/δ) is a transcription factor that is activated by endogenous fatty acid ligands and by synthetic agonists. Its role in the regulation of skeletal muscle fatty acid catabolism, glucose homeostasis, and cellular differentiation has been established in multiple studies. On the contrary, a role for PPARβ/δ in tumorigenesis is less clear because there are contradictory reports in the literature. However, the majority of these studies have not examined the role of PPARβ/δ in the tumor stroma. Recent evidence suggests that stromal PPARβ/δ regulates tumor endothelial cell proliferation and promotes differentiation leading to the properly orchestrated events required for tumor blood vessel formation. This review briefly summarizes the significance of these studies that may provide clues to help explain the reported discrepancies in the literature regarding the role of PPARβ/δ in tumorigenesis.http://dx.doi.org/10.1155/2008/534294
spellingShingle Rolf Müller
Martin Kömhoff
Jeffrey M. Peters
Sabine Müller-Brüsselbach
A Role for PPARβ/δ in Tumor Stroma and Tumorigenesis
PPAR Research
title A Role for PPARβ/δ in Tumor Stroma and Tumorigenesis
title_full A Role for PPARβ/δ in Tumor Stroma and Tumorigenesis
title_fullStr A Role for PPARβ/δ in Tumor Stroma and Tumorigenesis
title_full_unstemmed A Role for PPARβ/δ in Tumor Stroma and Tumorigenesis
title_short A Role for PPARβ/δ in Tumor Stroma and Tumorigenesis
title_sort role for pparβ δ in tumor stroma and tumorigenesis
url http://dx.doi.org/10.1155/2008/534294
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