The transcription factor Egr1 is a direct regulator of multiple tumor suppressors including TGFβ1, PTEN, p53, and fibronectin

被引:297
作者
Baron, V
Adamson, ED
Calogero, A
Ragona, G
Mercola, D [1 ]
机构
[1] Univ Calif Irvine, Dept Pathol, Irvine, CA 92017 USA
[2] Sidney Kimmel Canc Ctr, San Diego, CA USA
[3] Burnham Inst, La Jolla, CA 92037 USA
[4] Univ Rome, Rome, Italy
[5] Univ Calif San Diego, Rebecca & John Moores Canc Ctr, La Jolla, CA 92093 USA
关键词
suppressor network; anoikis; systems biology; prostate cancer; tumor progression;
D O I
10.1038/sj.cgt.7700896
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Recent studies are reviewed indicating that the transcription factor early growth response-1 (Egr1) is a direct regulator of multiple tumor suppressors including TGF beta 1, PTEN, p53, and fibronectin. The downstream pathways of these factors display multiple nodes of interaction with each other, suggesting the existence of a functional network of suppressor factors that serve to maintain normal growth regulation and resist the emergence of transformed variants. Paradoxically, Egr1 is oncogenic in prostate cancer. In the majority of these cancers, PTEN or p53 is inactive. It is suggested that these defects in the suppressor network allow for the unopposed induction of TGF beta 1 and fibronectin, which favor transformation and survival of prostate tumor epithelial cells, and explain the role of Egr1 in prostate cancer. Egr1 is a novel and logical target for intervention by gene therapy methods, and targeting methods are discussed.
引用
收藏
页码:115 / 124
页数:10
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