A key mediator of TGFβ-induced tumor invasion
A key mediator of TGFβ-induced tumor invasion
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DOI：
10.4161/cc.5.2.2311
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发表时间：
2006-01-16
期刊：
影响因子：
4.3
通讯作者：
Downward, J
中科院分区：
文献类型：
--
作者：
Michl, P;Downward, J
TGF β通路在人类癌发生中起着双重作用。一方面，TGF β因其抑制上皮细胞增殖和促进凋亡的能力而众所周知。然而，许多晚期癌症获得对TGF β的生长抑制作用的抗性，并对它作出反应，而不是促进增殖，侵袭和肿瘤进展。同源框转录因子CUTL 1，也称为CCAAT置换蛋白，CDP或Cux-1，参与正常胚胎发育和分化的控制。最近，我们发现CUTL 1是TGF β的转录靶点，并且是TGF β诱导的细胞迁移和侵袭的重要介质。此外，CUTL 1在各种上皮癌中高度表达，似乎与肿瘤分化和患者生存率呈负相关。因此，我们推测CUTL 1可能是TGF β在晚期癌症中促肿瘤作用的关键介质。
The TGF beta pathway plays a dual role in human carcinogenesis. On one hand, TGF beta is well known for its ability to inhibit epithelial cell proliferation and promote apoptosis. However, many advanced cancers acquire resistance to the growth-inhibitory effects of TGF beta and respond to it instead with promotion of proliferation, invasion and tumor progression. The homeobox transcription factor CUTL1, also known as CCAAT displacement protein, CDP or Cux-1, is involved in the control of normal embryonic development and differentiation. Recently, we found that CUTL1 is a transcriptional target of TGF beta and is an important mediator of the TGF beta-induced cell migration and invasion. In addition, CUTL1 is highly expressed in various epithelial cancers and seems to negatively correlate with tumor differentiation and patient survival. Therefore we postulate that CUTL1 might be a key mediator of the tumor-promoting effects of TGF beta in advanced cancers.