整合素连接激酶(ILK)在上皮-间质转化(EMT)中的作用机制

Dorota Gil , Dorota Ciołczyk-Wierzbicka , Joanna Dulińska-Litewka , Karolina Żwawa , James A. McCubrey , Piotr Laidler
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引用次数: 51

摘要

整合素连接激酶(Integrin linked kinase, ILK)是一种普遍表达的丝氨酸/苏氨酸蛋白激酶,是β1和β3整合素亚基的结合伙伴,是整合素受体的细胞质效应体,在功能上将它们与肌动蛋白细胞骨架连接。我们假设ILK是参与上皮-间质转化(EMT)的重要酶,这是癌症进展过程中的关键事件。常用的EMT分子标记包括N-cadherin和vimentin表达增加,β-catenin核定位,E-cadherin合成减少等。在这项研究中,我们能够证明N-cadherin在黑色素瘤细胞中的表达依赖于ILK信号和β-catenin向细胞核的易位。通过siRNA沉默ILK表达可显著抑制β-catenin的稳定和随后的核易位以及N-cadherin的表达。N-cadherin是EMT中的一个关键分子,在各种癌症侵袭过程中促进与成纤维细胞和内皮细胞的关联。这些结果允许我们谨慎地推测ILK在黑色素瘤EMT中整合素和钙粘蛋白之间的串扰中的重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The mechanism of contribution of integrin linked kinase (ILK) to epithelial-mesenchymal transition (EMT)
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