局灶黏附蛋白整合素连接激酶(ILK)在乳腺癌发病机制中起重要作用。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2020-12-01 DOI:10.1080/19336918.2020.1829263
Katerina Tsirtsaki, Vasiliki Gkretsi
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引用次数: 13

摘要

细胞-细胞外基质相互作用或局灶黏附(FA)对组织稳态至关重要,但也与癌症有关。整合素连接激酶(Integrin-Linked Kinase, ILK)是一种丰富表达的FA蛋白,参与多种信号通路。在这里,我们回顾了目前关于ILK在乳腺癌(BC)中的作用的文献。文章包括体外和体内实验以及人类BC样本的研究。ILK通过沉默或药物抑制而衰减,导致细胞凋亡或抑制上皮向间质转化和细胞侵袭,而ILK过表达则抑制细胞凋亡并促进肿瘤生长和转移。最后,ILK在BC肿瘤中上调,其表达与肿瘤分级和转移有关。因此,ILK应被评价为潜在的抗癌药物靶点。
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The focal adhesion protein Integrin-Linked Kinase (ILK) as an important player in breast cancer pathogenesis.

Cell-extracellular matrix interactions, or focal adhesions (FA), are crucial for tissue homeostasis but are also implicated in cancer. Integrin-Linked Kinase (ILK) is an abundantly expressed FA protein involved in multiple signaling pathways. Here, we reviewed the current literature on the role of ILK in breast cancer (BC). Articles included in vitro and in vivo experiments as well as studies in human BC samples. ILK attenuation via silencing or pharmaceutical inhibition, leads to apoptosis or inhibition of epithelial-to-mesenchymal transition, and cell invasion whereas ILK overexpression suppresses anoikis and promotes tumor growth and metastasis. Finally, ILK is upregulated in BC tumors and its expression is associated with grade, and metastasis. Therefore, ILK should be evaluated as a potential anti-cancer pharmaceutical target.

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CiteScore
7.20
自引率
4.30%
发文量
567
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