Dumont N, Arteaga C L
Vanderbilt University School of Medicine and Vanderbilt-Ingram Cancer Center, 22nd Avenue South, Nashville, TN 37232-5536, USA.
Breast Cancer Res. 2000;2(2):125-32. doi: 10.1186/bcr44. Epub 2000 Feb 21.
The transforming growth factor (TGF)-betas are potent growth inhibitors of normal epithelial cells. In established tumor cell systems, however, the preponderant experimental evidence suggests that TGF-betas can foster tumor-host interactions that indirectly support the viability and/or progression of cancer cells. The timing of this 'TGF-beta switch' during the progressive transformation of epithelial cells is not clear. More recent evidence also suggests that autocrine TGF-beta signaling is operative in some tumor cells, and can also contribute to tumor invasiveness and metastases independent of an effect on nontumor cells. The dissociation of antiproliferative and matrix associated effects of autocrine TGF-beta signaling at a transcriptional level provides for a mechanism(s) by which cancer cells can selectively use this signaling pathway for tumor progression. Data in support of the cellular and molecular mechanisms by which TGF-beta signaling can accelerate the natural history of tumors will be reviewed in this section.
转化生长因子（TGF）-β是正常上皮细胞的强效生长抑制剂。然而，在已建立的肿瘤细胞系统中，大量实验证据表明，TGF-β可促进肿瘤与宿主的相互作用，间接支持癌细胞的存活和/或进展。上皮细胞进行性转化过程中这种“TGF-β转换”的时机尚不清楚。最近的证据还表明，自分泌TGF-β信号在某些肿瘤细胞中起作用，并且也可独立于对非肿瘤细胞的影响而促进肿瘤侵袭和转移。自分泌TGF-β信号在转录水平上抗增殖和基质相关效应的解离为癌细胞选择性利用该信号通路促进肿瘤进展提供了一种机制。本节将综述支持TGF-β信号可加速肿瘤自然进程的细胞和分子机制的数据。
