Transforming growth factor-beta and breast cancer: Tumor promoting effects of transforming growth factor-beta.
Transforming growth factor-beta and breast cancer: Tumor promoting effects of transforming growth factor-beta.
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DOI：
10.1186/bcr44
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发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Arteaga CL
中科院分区：
文献类型：
--
作者：
Dumont N;Arteaga CL
转化生长因子（transforming growth factor，TGF）-βs是一种有效的上皮细胞生长抑制因子。然而，在已建立的肿瘤细胞系统中，占优势的实验证据表明，TGF-βs可以促进肿瘤-宿主相互作用，间接支持癌细胞的活力和/或进展。上皮细胞进行性转化过程中这种“TGF-β开关”的时间尚不清楚。最近的证据还表明，自分泌TGF-β信号传导在一些肿瘤细胞中起作用，并且还可以独立于对非肿瘤细胞的影响而促进肿瘤侵袭和转移。在转录水平上自分泌TGF-β信号传导的抗增殖和基质相关效应的解离提供了一种机制，癌细胞可以通过该机制选择性地使用该信号传导途径进行肿瘤进展。支持TGF-β信号传导可加速肿瘤自然病程的细胞和分子机制的数据将在本节中进行综述。
The transforming growth factor (TGF)-βs are potent growth inhibitors of normal epithelial cells. In established tumor cell systems, however, the preponderant experimental evidence suggests that TGF-βs can foster tumor-host interactions that indirectly support the viability and/or progression of cancer cells. The timing of this 'TGF-β switch' during the progressive transformation of epithelial cells is not clear. More recent evidence also suggests that autocrine TGF-β 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-β 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-β signaling can accelerate the natural history of tumors will be reviewed in this section.
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