Stover Daniel G, Bierie Brian, Moses Harold L
Department of Cancer Biology, Vanderbilt University, Nashville, TN 37232, USA.
J Cell Biochem. 2007 Jul 1;101(4):851-61. doi: 10.1002/jcb.21149.
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.
转化生长因子-β（TGF-β）的激活形式是上皮细胞自主性肿瘤起始、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信号的丧失可导致一种“激活的”微环境，这种微环境支持甚至启动相邻上皮细胞的转化。癌症中的TGF-β信号可通过涉及配体激活和该信号通路中包括受体和下游效应器在内的必需成分表达的机制来调节。肿瘤微环境中的TGF-β信号通过体内上皮细胞自主性和相互依赖的基质-上皮相互作用，对癌的起始、进展和转移产生显著影响。
