Regulation of EMT by TGFβ in cancer

被引:470
作者
Heldin, Carl-Henrik [1 ]
Vanlandewijck, Michael [1 ]
Moustakas, Aristidis [1 ,2 ]
机构
[1] Uppsala Univ, Ludwig Inst Canc Res, SE-75124 Uppsala, Sweden
[2] Uppsala Univ, Sci Life Lab, Dept Med Biochem & Microbiol, SE-75123 Uppsala, Sweden
来源
FEBS LETTERS | 2012年 / 586卷 / 14期
基金
瑞典研究理事会;
关键词
Cancer stem cell; Epithelial-mesenchymal transition; MAPK; Metastasis; Smad; TGF beta; EPITHELIAL-MESENCHYMAL TRANSITION; SUPERFAMILY SIGNALING PATHWAYS; MIR-200; FAMILY; E-CADHERIN; PROMOTES METASTASIS; FIBROBLASTS DERIVE; CELL INVASIVENESS; BONE METASTASIS; GENE-EXPRESSION; REPRESSORS ZEB1;
D O I
10.1016/j.febslet.2012.02.037
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) suppresses tumor formation since it inhibits cell growth and promotes apoptosis. However, in advanced cancers TGF beta elicits tumor promoting effects through its ability to induce epithelial-mesenchymal transition (EMT) which enhances invasiveness and metastasis; in addition, TGF beta exerts tumor promoting effects on non-malignant cells of the tumor, including suppression of immune surveillance and stimulation of angiogenesis. TGF beta promotes EMT by transcriptional and posttranscriptional regulation of a group of transcription factors that suppresses epithelial features, such as expression of components of cell junctions and polarity complexes, and enhances mesenchymal features, such as production of matrix molecules and several cytokines and growth factors that stimulate cell migration. The EMT program has certain similarities with the stem cell program. Inducers and effectors of EMT are interesting targets for the development of improved diagnosis, prognosis and therapy of cancer. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:1959 / 1970
页数:12
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