TGF-β and epithelial-to-mesenchymal transitions

被引:1356
作者
Zavadil, J
Böttinger, EP
机构
[1] NYU, Sch Med, Dept Pathol, New York, NY 10016 USA
[2] NYU, Sch Med, Inst Canc, New York, NY 10016 USA
[3] Mt Sinai Sch Med, Dept Med, New York, NY 10029 USA
关键词
Smad; metastasis; fibrosis; cancer; signal transduction; mesenchyme;
D O I
10.1038/sj.onc.1208927
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
Remarkable phenotype plasticity of epithelial cells underlies morphogenesis, epithelial repair and tumor invasiveness. Detailed understanding of the contextual cues and molecular mediators that control epithelial plasticity will be required in order to develop viable therapeutic approaches targeting epithelial-to-mesenchymal transition (EMT), an advanced manifestation of epithelial plasticity. Members of the transforming growth factor (TGF-beta) family of growth factors can initiate and maintain EMT in a variety of biological systems and pathophysiological context by activating major signaling pathways and transcriptional regulators integrated in extensive signaling networks. Here we will review the distinct physiological contexts of EMT and the underlying molecular signaling networks controlled by TGF-beta.
引用
收藏
页码:5764 / 5774
页数:11
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