A delicate balance:: TGF-β and the tumor microenvironment
A delicate balance:: TGF-β and the tumor microenvironment
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DOI：
10.1002/jcb.21149
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发表时间：
2007-07-01
影响因子：
4
通讯作者：
Moses, Harold L.
中科院分区：
文献类型：
--
作者：
Stover, Daniel G.;Bierie, Brian;Moses, Harold L.
TGF-β 的激活形式是上皮细胞自主肿瘤发生、进展和转移的已知调节因子。最近的研究还表明，TGF-β 介导癌细胞与其局部肿瘤微环境之间的相互作用。具体而言，包括成纤维细胞和 T 细胞在内的基质成分中 TGF-β 信号传导的丧失可能会导致微环境“激活”，支持甚至启动相邻上皮细胞的转化。癌症中的 TGF-β 信号传导可以通过涉及配体激活和通路内重要成分表达（包括受体和下游效应器）的机制进行调节。肿瘤微环境中的 TGF-β 信号传导通过体内上皮细胞自主和相互依赖的基质-上皮相互作用显着影响癌症的发生、进展和转移。
The activated form of TGF-beta is a known regulator of epithelial cell autonomous tumor initiation, progression, and metastasis. Recent Studies have also indicated that TGF-beta mediates interactions between cancer cells and their local tumor microenvironment. Specifically, the loss of TGF-beta signaling in stromal components including fibroblasts and T-cells can result in an "activated" microenvironment that supports and even initiates transformation of adjacent epithelial cells. TGF-beta signaling in cancer can be regulated through mechanisms involving ligand activation and expression of essential components within the pathway including the receptors and downstream effectors. TGF-beta signaling in the tumor microenvironment significantly impacts carcinoma initiation, progression, and metastasis via epithelial cell autonomous and interdependent stromal-epithelial interactions in vivo.