Gallo L H, Ko J, Donoghue D J
a Department of Chemistry and Biochemistry , University of California San Diego , La Jolla , CA , USA.
b Moores UCSD Cancer Center , University of California San Diego , La Jolla , CA , USA.
Cell Cycle. 2017 Apr 3;16(7):634-648. doi: 10.1080/15384101.2017.1288326. Epub 2017 Feb 6.
Ubiquitination serves as a degradation mechanism of proteins, but is involved in additional cellular processes such as activation of NFκB inflammatory response and DNA damage repair. We highlight the E2 ubiquitin conjugating enzymes, E3 ubiquitin ligases and Deubiquitinases that support the metastasis of a plethora of cancers. E3 ubiquitin ligases also modulate pluripotent cancer stem cells attributed to chemotherapy resistance. We further describe mutations in E3 ubiquitin ligases that support tumor proliferation and adaptation to hypoxia. Thus, this review describes how tumors exploit members of the vast ubiquitin signaling pathways to support aberrant oncogenic signaling for survival and metastasis.
泛素化是一种蛋白质降解机制，但它还参与其他细胞过程，如激活NFκB炎症反应和DNA损伤修复。我们重点介绍了支持多种癌症转移的E2泛素结合酶、E3泛素连接酶和去泛素化酶。E3泛素连接酶还调节与化疗耐药性相关的多能癌症干细胞。我们进一步描述了支持肿瘤增殖和适应缺氧的E3泛素连接酶中的突变。因此，本综述描述了肿瘤如何利用广泛的泛素信号通路成员来支持异常的致癌信号，以实现生存和转移。
