Ludwig Institute for Cancer Research, Uppsala University, Box 595, SE-751 24 Uppsala, Sweden.
FEBS Lett. 2012 Jul 4;586(14):1959-70. doi: 10.1016/j.febslet.2012.02.037. Epub 2012 Feb 28.
Transforming growth factor-β (TGFβ) suppresses tumor formation since it inhibits cell growth and promotes apoptosis. However, in advanced cancers TGFβ elicits tumor promoting effects through its ability to induce epithelial-mesenchymal transition (EMT) which enhances invasiveness and metastasis; in addition, TGFβ exerts tumor promoting effects on non-malignant cells of the tumor, including suppression of immune surveillance and stimulation of angiogenesis. TGFβ 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.
转化生长因子-β（TGFβ）通过抑制细胞生长和促进细胞凋亡来抑制肿瘤形成。然而，在晚期癌症中，TGFβ 通过诱导上皮-间充质转化（EMT）来发挥促进肿瘤的作用，这增强了侵袭性和转移能力；此外，TGFβ 对肿瘤的非恶性细胞也具有促进肿瘤的作用，包括抑制免疫监视和刺激血管生成。TGFβ 通过转录和转录后调控一组转录因子来促进 EMT，这些转录因子抑制上皮特征，如细胞连接和极性复合物成分的表达，并增强间充质特征，如基质分子和几种细胞因子和生长因子的产生，这些因子刺激细胞迁移。EMT 程序与干细胞程序具有某些相似之处。EMT 的诱导剂和效应物是开发改善癌症诊断、预后和治疗的有趣靶点。
