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P120 and E-cadherin: Double-edged swords in tumor metastasis.
Seminars in Cancer Biology ( IF 14.5 ) Pub Date : 2019-07-29 , DOI: 10.1016/j.semcancer.2019.07.020
Jan-Hendrik Venhuizen 1 , Femke J C Jacobs 1 , Paul N Span 2 , Mirjam M Zegers 1
Affiliation  

Cell-cell adhesion by adherens junctions controls proliferation and cell polarization and is crucial to maintain epithelial architecture and homeostasis. Downregulation of two of the main components of adherens junctions, E-cadherin and p120, is an often recurring hallmark of carcinomas, causing loss of polarity and increased proliferation, survival and invasion of epithelial cells. On the other hand, tumor-promoting effects of both E-cadherin and p120 have been reported, substantiated by sustained, or even elevated expression of these molecules in many cancers. In this review, we will discuss how expression regulation by EMT, E-cadherin cleavage or p120 isoform expression can contribute to either tumor-supressing or tumor-promoting processes. Furthermore, we will focus on the contradictory functions of E-cadherin and p120 in the different phases of tumor progression, from carcinoma in situ up to the formation of distant metastasis. Finally, we will discuss the possibilities and challenges when using either protein as a biomarker.



中文翻译:

P120和E-cadherin:肿瘤转移中的双刃剑。

细胞通过粘附连接的粘附控制增殖和细胞极化,对于维持上皮结构和体内平衡至关重要。粘附连接的两个主要成分,E-钙粘着蛋白和p120的下调通常是癌症的复发标志,导致极性丧失并增加上皮细胞的增殖,存活和侵袭。另一方面,据报道,E-钙粘着蛋白和p120均具有促进肿瘤的作用,这些作用在许多癌症中持续甚至升高的表达得以证实。在这篇综述中,我们将讨论通过EMT,E-钙粘蛋白裂解或p120亚型表达调控的表达如何促进肿瘤抑制或促进肿瘤的过程。此外,原位直至远处转移的形成。最后,我们将讨论使用两种蛋白质作为生物标记物时的可能性和挑战。

更新日期:2019-07-29
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