To Live or to Die: Prosurvival Activity of PPARγ in Cancers

被引：107

作者：

Wang, Y. Lynn ^{[1
]}

Miao, Qi ^{[1
]}

机构：

[1] Weill Cornell Med Coll, Dept Pathol & Lab Med, Mol Hematopathol Lab, New York, NY 10065 USA

来源：

PPAR RESEARCH | 2008年 / 2008卷

关键词：

D O I：

10.1155/2008/209629

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

The role of PPAR gamma in tumorigenesis is controversial. In this article, we review and analyze literature from the past decade that highlights the potential proneoplastic activity of PPAR gamma. We discuss the following five aspects of the nuclear hormone receptor and its agonists: (1) relative expression of PPAR gamma in human tumor versus normal tissues; (2) receptor-dependent proneoplastic effects; (3) impact of PPAR gamma and its agonists on tumors in animal models; (4) clinical trials of thiazolidinediones (TZDs) in human malignancies; (5) TZDs as chemopreventive agents in epidemiology studies. The focus is placed on the most relevant in vivo animal models and human data. In vitro cell line studies are included only when the effects are shown to be dependent on the PPAR gamma receptor. Copyright (C) 2008 Y. Lynn Wang and Q. Miao.

引用

页数：13

共 78 条

[1] Biosynthesis of 15-deoxy-Δ12,14-PGJ2 and the litigation of PPARγ [J].

Bell-Parikh, LC ;

Ide, T ;

Lawson, JA ;

McNamara, P ;

Reilly, M ;

FitzGerald, GA .

JOURNAL OF CLINICAL INVESTIGATION, 2003, 112 (06) :945-955

[2] Peroxisome proliferator-activated receptor-γ agonists suppress adrenocortical tumor cell proliferation and induce differentiation [J].

Betz, MJ ;

Shapiro, I ;

Fassnacht, M ;

Hahner, S ;

Reincke, M ;

Beuschlein, F .

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2005, 90 (07) :3886-3896

[3] Antitumorigenic effects of peroxisome proliferator-activated receptor-γ in non-small-cell lung cancer cells are mediated by suppression of cyclooxygenase-2 via inhibition of nuclear factor-κB [J].

Bren-Mattison, Yvette ;

Meyer, Amy M. ;

Van Putten, Vicki ;

Li, Howard ;

Kuhn, Katherine ;

Stearman, Robert ;

Weiser-Evans, Mary ;

Winn, Robert A. ;

Heasley, Lynn E. ;

Nemenoff, Raphael A. .

MOLECULAR PHARMACOLOGY, 2008, 73 (03) :709-717

[4] 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

[5]

Chang Young Woon, 2004, Korean J Gastroenterol, V43, P291

[6]

Chinery R, 1999, CANCER RES, V59, P2739

[7] 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

[8] Oncogenic alterations of metabolism [J].

Dang, CV ;

Semenza, GL .

TRENDS IN BIOCHEMICAL SCIENCES, 1999, 24 (02) :68-72

[9] 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

[10] Clinical pharmacokinetics of pioglitazone [J].

Eckland, DA ;

Danhof, M .

EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES, 2000, 108 :S234-S242

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