PPAR trilogy from metabolism to cancer

被引:31
作者
Nahlé, Z [1 ]
机构
[1] Washington Univ, Ctr Human Nutr, Dept Med, St Louis, MO 63110 USA
关键词
peroxisome proliferator-activated receptor; apoptosis; metabolism; cancer; differentiation; transcription factors; peroxisome proliferator-activated receptor agonist;
D O I
10.1097/01.mco.0000134360.30911.bb
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review This review highlights recent advances related to malignancies in the field of peroxisome proliferator-activated receptors (PPARs). It also discusses the implications of cancer research and therapy. Recent findings In the last few years, genetic evidence has implicated the PPARs, specifically PPARgamma and PPARbeta/delta, in tumorigenesis. Also, new insights into the regulation of the nuclear hormone receptors have emerged. Summary Exciting research in PPAR biology has established these nuclear factors as key regulators of metabolism and energy homeostasis. Evidence indicates that PPARs can also affect the pathogenesis and development of tumors. However, the type of effects observed thus far appears to depend on the experimental context. As a result, the findings are generating much debate, as PPAR agonists are widespread targets in the treatment of metabolic disorders such as diabetes and dyslipidemia. Here, we summarize the most recent advances in this field, outline the conflicting reports and discuss their overall implications in cancer research.
引用
收藏
页码:397 / 402
页数:6
相关论文
共 66 条
[1]  
Auwerx J, 1999, CELL, V97, P161
[2]   Effects of peroxisome proliferator-activated receptor δ on placentation, adiposity, and colorectal cancer [J].
Barak, Y ;
Liao, D ;
He, WM ;
Ong, ES ;
Nelson, MC ;
Olefsky, JM ;
Boland, R ;
Evans, RM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (01) :303-308
[3]   SUPPRESSION OF LIVER-CELL APOPTOSIS IN-VITRO BY THE NONGENOTOXIC HEPATOCARCINOGEN AND PEROXISOME PROLIFERATOR NAFENOPIN [J].
BAYLY, AC ;
ROBERTS, RA ;
DIVE, C .
JOURNAL OF CELL BIOLOGY, 1994, 125 (01) :197-203
[4]   HEPATIC PEROXISOME PROLIFERATION IN RODENTS AND ITS SIGNIFICANCE FOR HUMANS [J].
BENTLEY, P ;
CALDER, I ;
ELCOMBE, C ;
GRASSO, P ;
STRINGER, D ;
WIEGAND, HJ .
FOOD AND CHEMICAL TOXICOLOGY, 1993, 31 (11) :857-907
[5]   Use of the peroxisome proliferator-activated receptor (PPAR) γ ligand troglitazone as treatment for refractory breast cancer:: a phase II study [J].
Burstein, HJ ;
Demetri, GD ;
Mueller, E ;
Sarraf, P ;
Spiegelman, BM ;
Winer, EP .
BREAST CANCER RESEARCH AND TREATMENT, 2003, 79 (03) :391-397
[6]   Apoptosis induced by activation of peroxisome-proliferator activated receptor-gamma is associated with Bcl-2 and Nf-kB in human colon cancer [J].
Chen, GG ;
Lee, JFY ;
Wang, SH ;
Chan, UPF ;
Ip, PC ;
Lau, WY .
LIFE SCIENCES, 2002, 70 (22) :2631-2646
[7]   15-deoxy-Δ12,14-prostaglandin J2-induced apoptosis does not require PPARγ in breast cancer cells [J].
Clay, CE ;
Monjazeb, A ;
Thorburn, J ;
Chilton, FH ;
High, KP .
JOURNAL OF LIPID RESEARCH, 2002, 43 (11) :1818-1828
[8]   Magnitude of peroxisome proliferator-activated receptor-γ activation is associated with important and seemingly opposite biological responses in breast cancer cells [J].
Clay, CE ;
Namen, AM ;
Atsumi, G ;
Trimboli, AJ ;
Fonteh, AN ;
High, KP ;
Chilton, FH .
JOURNAL OF INVESTIGATIVE MEDICINE, 2001, 49 (05) :413-420
[9]   Loss of the peroxisome proliferation-activated receptor gamma (PPARγ) does not affect mammary development and propensity for tumor formation but leads to reduced fertility [J].
Cui, Y ;
Miyoshi, K ;
Claudio, E ;
Siebenlist, UK ;
Gonzalez, FJ ;
Flaws, J ;
Wagner, KU ;
Hennighausen, L .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (20) :17830-17835
[10]   A phase II trial with rosiglitazone in liposarcoma patients [J].
Debrock, G ;
Vanhentenrijk, V ;
Sciot, R ;
Debiec-Rychter, M ;
Oyen, R ;
Van Oosterom, A .
BRITISH JOURNAL OF CANCER, 2003, 89 (08) :1409-1412