Kretzschmar M
Ruttenberg Cancer Center, NYU-Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
Breast Cancer Res. 2000;2(2):107-15. doi: 10.1186/bcr42. Epub 2000 Feb 21.
Transforming growth factor-beta (TGF-beta) is a tumor suppressor, the function of which is compromised in many types of human cancer, including breast cancer. The tumor suppressive effects of TGF-beta are caused by potent inhibition of cell proliferation due to cell cycle arrest in the G1 phase. Such antiproliferative responses are mediated by a signaling system that includes two types of cell surface receptors and intracellular signal transducers, the SMAD proteins. Different molecular mechanisms can lead to loss of antiproliferative TGF-beta responses in tumor cells, including mutations in components of the signaling system and inhibition of the SMAD signaling pathway by aberrant activities of various regulatory molecules. Some of these mechanisms will be discussed, with emphasis on their potential involvement in breast tumorigenesis.
转化生长因子-β（TGF-β）是一种肿瘤抑制因子，其功能在包括乳腺癌在内的多种人类癌症中受到损害。TGF-β的肿瘤抑制作用是由于其通过使细胞周期停滞在G1期而有效抑制细胞增殖所致。这种抗增殖反应由一个信号系统介导，该信号系统包括两种类型的细胞表面受体和细胞内信号转导分子，即SMAD蛋白。不同的分子机制可导致肿瘤细胞中抗增殖TGF-β反应丧失，包括信号系统成分的突变以及各种调节分子的异常活性对SMAD信号通路的抑制。将讨论其中一些机制，重点是它们在乳腺肿瘤发生中的潜在作用。
