摘要
上皮-间质转化(EMT)在肿瘤转移过程中的促进细胞迁移和侵袭起着重要作用。一个EMT的标志是减少E-cadherin表达和间充质性状的获得,这是受核心EMT诱导转录因子的调控(EMT-TFS),如Snail/Slug、ZEB1/ZEB2,Twist1。EMT-TFs是极不稳定的蛋白质,其蛋白质含量受泛素-蛋白酶体系统(UPS)的严格控制。几个E3泛素连接酶已被证明在EMT的调控中发挥重要的作用,并且在这些连接酶的基因变异和变化已经在人类癌症中检测到。在这篇综述中,我们专注于EMT-TFS,描述癌症控制他们的活动和功能的UPS。对UPS在EMT的调节作用有更深的了解,将为制定有效的抗转移药物调节恶性过程介导EMT提供有价值的信息。
关键词: 去泛素化酶抑制剂(DUB),E3泛素连接酶,上皮-间质转化(EMT),Snail, Slug, Twis,泛素蛋白酶体系统(UPS),ZEB转录因子。
Current Cancer Drug Targets
Title:Regulation of Epithelial-Mesenchymal Transition by E3 Ubiquitin Ligases and Deubiquitinase in Cancer
Volume: 16 Issue: 2
Author(s): Yasumichi Inoue, Yuka Itoh, Koichi Sato, Fumihiro Kawasaki, Chihiro Sumita, Takahito Tanaka, Daisuke Morishita and Hidetoshi Hayashi
Affiliation:
关键词: 去泛素化酶抑制剂(DUB),E3泛素连接酶,上皮-间质转化(EMT),Snail, Slug, Twis,泛素蛋白酶体系统(UPS),ZEB转录因子。
摘要: Epithelial-mesenchymal transition (EMT) plays an important role in the development of tumor metastases by facilitating cell migration and invasion. One of the hallmarks of EMT is the diminished expression of E-cadherin and gain of mesenchymal traits, which are regulated by core EMT-inducing transcriptional factors (EMT-TFs), such as Snail/Slug, ZEB1/ZEB2, and Twist1. EMT-TFs are known to be extremely labile proteins, and their protein levels are tightly controlled by the ubiquitin-proteasome system (UPS). Several E3 ubiquitin ligases have been shown to play crucial roles in the regulation of EMT, and genetic aberrations and alterations in these ligases have been detected in human cancer. In this review, we focused on EMT-TFs, describing the UPS controlling their activities and functions in cancer. A deeper understanding of the role of UPS in the regulation of EMT will provide valuable information for the development of effective anti-metastatic drugs to modulate the malignant processes mediated by EMT.
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Yasumichi Inoue, Yuka Itoh, Koichi Sato, Fumihiro Kawasaki, Chihiro Sumita, Takahito Tanaka, Daisuke Morishita and Hidetoshi Hayashi , Regulation of Epithelial-Mesenchymal Transition by E3 Ubiquitin Ligases and Deubiquitinase in Cancer, Current Cancer Drug Targets 2016; 16 (2) . https://dx.doi.org/10.2174/1568009616666151112122126
DOI https://dx.doi.org/10.2174/1568009616666151112122126 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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