Regulation of the actin cytoskeleton in cancer cell migration and invasion
Regulation of the actin cytoskeleton in cancer cell migration and invasion
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DOI：
10.1016/j.bbamcr.2006.07.001
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发表时间：
2007-05-01
影响因子：
5.1
通讯作者：
Condeelis, John
中科院分区：
文献类型：
--
作者：
Yamaguchi, Hideki;Condeelis, John
恶性癌细胞利用其固有的迁移能力侵入邻近组织和脉管系统，并最终转移。细胞迁移是由响应迁移和趋化刺激而形成的膜突起发起的多步骤过程的总和。膜突的驱动力是膜下肌动蛋白丝的局部聚合。最近，一些研究表明，在侵袭性和转移性癌细胞中，连接迁移信号和肌动蛋白细胞骨架的分子上调。本文从肌动蛋白细胞骨架的关键调控蛋白的功能等方面，综述了近年来肿瘤细胞利用板足和侵足形成侵袭性突起的分子机制的研究进展；WASP家族蛋白，Arp2/3复合物，lim激酶，cofilin，和接触蛋白。(c) 2006 Elsevier B.V.版权所有
Malignant cancer cells utilize their intrinsic migratory ability to invade adjacent tissues and the vasculature, and ultimately to metastasize. Cell migration is the sum of multi-step processes initiated by the formation of membrane protrusions in response to migratory and chemotactic stimuli. The driving force for membrane protrusion is localized polymerization of submembrane actin filaments. Recently, several studies revealed that molecules that link migratory signals to the actin cytoskeleton are upregulated in invasive and metastatic cancer cells. In this review, we summarize recent progress on molecular mechanisms of formation of invasive protrusions used by tumor cells, such as lamellipodia and invadopodia, with regard to the functions of key regulatory proteins of the actin cytoskeleton; WASP family proteins, Arp2/3 complex, LIM-kinase, cofilin, and cortactin. (c) 2006 Elsevier B.V. All rights reserved.