TWEAK and Fn14: New molecular targets for cancer therapy?

被引：58

作者：

Winkles, JA

Tran, NL

Berens, ME

机构：

[1] Univ Maryland, Sch Med, Dept Surg, Baltimore, MD 21201 USA

[2] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA

[3] Univ Maryland, Sch Med, Greenebaum Canc Ctr, Baltimore, MD 21201 USA

[4] Translat Genom Res Inst, Neurogenom Div, Phoenix, AZ 85004 USA

来源：

CANCER LETTERS | 2006年 / 235卷 / 01期

关键词：

TNF; TWEAK; Fn14; cancer tumor; endothelial cell; angiogenesis;

D O I：

10.1016/j.canlet.2005.03.048

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a member of the tumor necrosis factor (TNF) superfamily of structurally related cytokines. Full-length, membrane-anchored TWEAK can be found on the surface of many cell types and a smaller, biologically active form, generated via proteolytic processing, has also been detected in the extracellular milieu. TWEAK acts via binding to a recently identified TNF receptor superfamily member named fibroblast growth factor-inducible 14 (Fn14). It has been demonstrated that TWEAK binding to the Fn14 receptor, or constitutive Fn14 overexpression, activates the nuclear factor-KB signaling pathway, which is known to play an important role in immune and inflammatory processes, oncogenesis, and cancer therapy resistance. In this article, we review recent studies indicating that TWEAK and Fn14 may be potential regulators of human tumorigenesis. (c) 2005 Elsevier Ireland Ltd. All rights reserved.

引用

收藏

页码：11 / 17

页数：7

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