Dynamic interplay between adhesion surfaces in carcinomas: Cell-cell and cell-matrix crosstalk.

Y. Smith, S. Vellanki, A. Hopkins
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引用次数: 8

Abstract

Cell-cell and cell-matrix signaling and communication between adhesion sites involve mechanisms which are required for cellular functions during normal development and homeostasis; however these cellular functions and mechanisms are often deregulated in cancer. Aberrant signaling at cell-cell and cell-matrix adhesion sites often involves downstream mediators including Rho GTPases and tyrosine kinases. This review discusses these molecules as putative mediators of cellular crosstalk between cell-cell and cell-matrix adhesion sites, in addition to their attractiveness as therapeutic targets in cancer. Interestingly, inter-junctional crosstalk mechanisms are frequently typified by the way in which bacterial and viral pathogens opportunistically infect or intoxicate mammalian cells. This review therefore also discusses the concept of learning from pathogen-host interaction studies to better understand coordinated communication between cell-cell and cell-matrix adhesion sites, in addition to highlighting the potential therapeutic usefulness of exploiting pathogens or their products to tap into inter-junctional crosstalk. Taken together, we feel that increased knowledge around mechanisms of cell-cell and cell-matrix adhesion site crosstalk and consequently a greater understanding of their therapeutic targeting offers a unique opportunity to contribute to the emerging molecular revolution in cancer biology.
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癌细胞粘附表面的动态相互作用:细胞-细胞和细胞-基质串扰。
细胞-细胞和细胞-基质之间的信号传导和粘附位点之间的通信涉及正常发育和体内平衡过程中细胞功能所需的机制;然而,这些细胞功能和机制在癌症中往往不受控制。细胞-细胞和细胞-基质粘附位点的异常信号通常涉及下游介质,包括Rho gtpase和酪氨酸激酶。这篇综述讨论了这些分子作为细胞-细胞和细胞-基质粘附位点之间细胞串扰的假定介质,以及它们作为癌症治疗靶点的吸引力。有趣的是,连接间串扰机制通常以细菌和病毒病原体机会性感染或中毒哺乳动物细胞的方式为典型。因此,本文还讨论了从病原体-宿主相互作用研究中学习的概念,以更好地了解细胞-细胞和细胞-基质粘附位点之间的协调通信,此外还强调了利用病原体或其产物利用连接间串扰的潜在治疗用途。综上所述,我们认为增加对细胞-细胞和细胞-基质粘附位点串音机制的了解,从而更好地了解它们的治疗靶向,为癌症生物学中新兴的分子革命提供了一个独特的机会。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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