New insights into Nm23 control of cell adhesion and migration
New insights into Nm23 control of cell adhesion and migration
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DOI：
10.1023/a:1023450008347
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发表时间：
2003-02-01
影响因子：
3
通讯作者：
Block, MR
中科院分区：
文献类型：
--
作者：
Fournier, HN;Albigès-Rizo, C;Block, MR
Nm23/NDP激酶在控制细胞迁移和转移中作用的分子机制已经被研究。我们在分子水平上对细胞迁移的理解的最新进展为我们提供了一些可能的Nm23作为转移抑制因子的线索。对文献的筛选表明，NDP激酶具有多效性。通过改变细胞骨架组织和蛋白运输，一些NDP激酶亚型可能间接促进某些细胞类型与细胞外基质的黏附。相反，Nm23调节细胞表面整合素受体和基质金属蛋白酶的表达，从而直接控制细胞的黏附机制。最后，最近发现Nm23-H2与1整合素介导的细胞黏附的负调控因子ICAP-1之间的相互作用，ICAP-1针对片状脂膜和细胞突起，表明Nm23-H2/ICAP-1复合体在整合素信号转导中发挥作用，并在迁移和扩散之间发挥微调作用。
The molecular mechanisms underlying the role of Nm23/NDP kinase in controlling cell migration and metastasis have been investigated. The recent progress in our understanding of cell migration at a molecular level gives us some clues to the putative Nm23 function as a suppressor of metastasis. Screening of the literature indicates that NDP kinases have pleiotropic effects. By modifying cytoskeleton organization and protein trafficking, some NDP kinase isoforms may indirectly promote adhesion to the extracellular matrix in some cell types. Conversely, Nm23 regulates cell surface expression of integrin receptors and matrix metallo-proteases, and thus directly controls the cell adhesion machinery. Finally, the recent discovery of the interaction between Nm23-H2 and the negative regulator of 1 integrin-mediated cell adhesion, ICAP-1, which targets the kinase to lamellipodia and cell protrusions, suggests that the Nm23-H2/ICAP-1 complex plays a role in integrin signaling, and exerts a fine-tuning between migration and spreading.