Transforming growth factor-beta signaling and tumor angiogenesis

被引：99

作者：

Pardali, Evangelia ^{[1
]}

ten Dijke, Peter ^{[1
]}

机构：

[1] Leiden Univ, Med Ctr, Dept Mol Cell Biol, NL-2300 RC Leiden, Netherlands

来源：

FRONTIERS IN BIOSCIENCE-LANDMARK | 2009年 / 14卷

关键词：

TGF-beta; BMP; Smad; Tumor; Angiogenesis; Endoglin; ALK; HHT; Review; HEREDITARY HEMORRHAGIC TELANGIECTASIA; BONE MORPHOGENETIC PROTEIN-2; HUMAN BREAST-CANCER; ENDOTHELIAL-CELL PROLIFERATION; RECOMBINANT SOLUBLE BETAGLYCAN; RECEPTOR-LIKE KINASE-1; MICE LACKING ENDOGLIN; YOLK-SAC VASCULATURE; HUMAN SOLID TUMORS; TGF-BETA;

D O I：

10.2741/3573

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Transforming growth factor-beta (TGF-beta) family members are secreted multifunctional cytokines that play pivotal roles in development and disease. The prototypic member of this family, TGF-beta, plays a dual role in carcinogenesis, acting as a tumor suppressor in early stages and as tumor promoter in late stages of tumor progression. Numerous studies support the notion that pathological angiogenesis is one of the hallmarks of cancer. Tumor angiogenesis is regulated by a network of growth factors, including members of the TGF-beta family. TGFbeta acts in a context-dependent manner and can either stimulate or inhibit tumor angiogenesis. In this review, we discuss our current understanding on how TGF-beta family members affect endothelial and smooth muscle cell function and how perturbed TGF-beta signaling may contribute to tumor angiogenesis and tumor progression.

引用

页码：4848 / 4861

页数：14

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