TRIM21 mediates ubiquitination of Snail and modulates epithelial to mesenchymal transition in breast cancer cells
TRIM21 mediates ubiquitination of Snail and modulates epithelial to mesenchymal transition in breast cancer cells
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DOI：
10.1016/j.ijbiomac.2018.11.269
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发表时间：
2019-03-01
影响因子：
8.2
通讯作者：
Wan, Youzhong
中科院分区：
文献类型：
--
作者：
Jin, Yue;Zhang, Yu;Wan, Youzhong
在上皮细胞向间充质细胞转化（EMT）过程中，癌细胞的迁移和侵袭能力大大增强。TRIM21的缺失促进了MCF7和T47D细胞的迁移和侵袭，改变了EMT调控基因的表达。TRIM21与EMT的主调控因子Snail相互作用。TRIM21的过表达导致蜗牛的泛素化和蛋白体降解增加，而TRIM21的缺失则降低蜗牛的泛素化。重要的是，Snail的缺失抑制了TRIM21缺失所促进的MCF7和T47D细胞的迁移和侵袭。TRIM21的高水平表达与乳腺癌患者更长的总生存期相关。总之，我们的研究表明TRIM21通过介导Snail在乳腺癌细胞中的稳定性来调节EMT。(C) 2018 Elsevier B.V.版权所有
Migration and invasion of cancer cells are greatly increased during epithelial to mesenchymal transition (EMT). Depletion of TRIM21 promotes the migration and invasion of MCF7 and T47D cells, and changes the expression of genes that regulate EMT. TRIM21 interacts with Snail, a master regulator of EMT. Overexpression of TRIM21 leads to increased ubiquitination and proteosomal degradation of Snail, while depletion of TRIM21 decreases the ubiquitination of Snail. Importantly, depletion of Snail suppresses the increased migration and invasion of MCF7 and T47D cells promoted by depletion of TRIM21. High-level expression of TRIM21 is associated with longer overall survival in breast cancer. Together, our study demonstrates that TRIM21 modulates EMT by mediating the stability of Snail in breast cancer cells. (C) 2018 Elsevier B.V. All rights reserved.