The Wnt/β-catenin signaling pathway targets PPARγ activity in colon cancer cells

被引：134

作者：

Jansson, EÅ

Are, A

Greicius, G

Kuo, IC

Kelly, D

Arulampalam, V

Pettersson, S ^{[1
]}

机构：

[1] Karolinska Inst, Microbiol & Tumor Biol Ctr, S-17177 Stockholm, Sweden

[2] Natl Univ Singapore, Dept Paediat, Fac Med, Singapore 119074, Singapore

[3] Natl Univ Singapore, Dept Biochem, Fac Med, Singapore 119074, Singapore

[4] Rowett Res Inst, Gut Immunol Grp, Aberdeen AB21 9SB, Scotland

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2005年 / 102卷 / 05期

关键词：

colon epithelium; Wnt signaling; nuclear receptors; APC(Min) mice; T cell transcription factor 4;

D O I：

10.1073/pnas.0405928102

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Control of colon cell fate in adenocarcinomas is disrupted, in part, due to aberrant Wnt/beta-catenin signaling. The nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARgamma) has been implicated in the development of colon cancers. In the adenomatous polyposis coli multiple intestinal neoplasia (APC(Min)) mouse cancer model, PPARgamma expression in the colonic mucosa is markedly altered. In addition, PPARgamma protein levels are elevated, possibly through sequestration by activated beta-catenin in colon cancer cell lines. Induction of the Wnt/beta-catenin pathway by LiCl also elevated PPARgamma levels and induced PPARgamma-dependent reporter and endogenous target genes. Mechanistically, PPARgamma, through interactions with beta-catenin and T cell transcription factor (Tcf)-4, may be a determinant of cell fate and is likely a target of the Wnt pathway in cancer cells.

引用

页码：1460 / 1465

页数：6

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