Signal Transduction Pathways of EMT Induced by TGF-β, SHH, and WNT and Their Crosstalks.
Signal Transduction Pathways of EMT Induced by TGF-β, SHH, and WNT and Their Crosstalks.
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DOI：
10.3390/jcm5040041
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发表时间：
2016-03-28
影响因子：
3.9
通讯作者：
Xing J
中科院分区：
文献类型：
--
作者：
Zhang J;Tian XJ;Xing J
上皮细胞向间质转化（EMT）是发育、伤口愈合和癌症发展的关键步骤。它涉及转化生长因子-β (TGF-β)、Sonic Hedgehog （SHH）和WNT等信号通路的协同作用。这些信号通路相互串扰并汇聚到关键转录因子（如SNAIL1）上，以初始化和维持EMT过程。多信号通路串串在EMT中的功能作用是复杂的，因此仍有待探索。在这篇综述中，我们主要关注在肿瘤中促进或调节EMT的三种主要信号转导途径。我们讨论了网络结构，并简要概述了目前针对这三种信号转导途径的治疗策略和药物开发。最后，我们强调了系统生物学方法可以加速解构复杂网络和药物发现的过程。
Epithelial-to-mesenchymal transition (EMT) is a key step in development, wound healing, and cancer development. It involves cooperation of signaling pathways, such as transformation growth factor-β (TGF-β), Sonic Hedgehog (SHH), and WNT pathways. These signaling pathways crosstalk to each other and converge to key transcription factors (e.g., SNAIL1) to initialize and maintain the process of EMT. The functional roles of multi-signaling pathway crosstalks in EMT are sophisticated and, thus, remain to be explored. In this review, we focused on three major signal transduction pathways that promote or regulate EMT in carcinoma. We discussed the network structures, and provided a brief overview of the current therapy strategies and drug development targeted to these three signal transduction pathways. Finally, we highlighted systems biology approaches that can accelerate the process of deconstructing complex networks and drug discovery.