Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.
J Cell Sci. 2012 Dec 15;125(Pt 24):5917-26. doi: 10.1242/jcs.093732. Epub 2013 Feb 1.
Cells migrating on flat two-dimensional (2D) surfaces use actin polymerization to extend the leading edge of the plasma membrane during lamellipodia-based migration. This mode of migration is not universal; it represents only one of several mechanisms of cell motility in three-dimensional (3D) environments. The distinct modes of 3D migration are strongly dependent on the physical properties of the extracellular matrix, and they can be distinguished by the structure of the leading edge and the degree of matrix adhesion. How are these distinct modes of cell motility in 3D environments related to each other and regulated? Recent studies show that the same type of cell migrating in 3D extracellular matrix can switch between different leading edge structures. This mode-switching behavior, or plasticity, by a single cell suggests that the apparent diversity of motility mechanisms is integrated by a common intracellular signaling pathway that governs the mode of cell migration. In this Commentary, we propose that the mode of 3D cell migration is governed by a signaling axis involving cell-matrix adhesions, RhoA signaling and actomyosin contractility, and that this might represent a universal mechanism that controls 3D cell migration.
细胞在二维（2D）平面上迁移时，利用肌动蛋白聚合作用在片状伪足（lamellipodia）迁移过程中延伸质膜的前缘。这种迁移模式并非普遍存在；它只代表了细胞在三维（3D）环境中几种运动机制之一。3D 迁移的不同模式强烈依赖于细胞外基质的物理特性，并且可以通过前缘结构和基质黏附程度来区分。3D 环境中这些不同的细胞运动模式如何相互关联并受到调节？最近的研究表明，在 3D 细胞外基质中迁移的同种细胞可以在不同的前缘结构之间切换。单个细胞的这种模式转换行为或可塑性表明，运动机制的明显多样性是由一个共同的细胞内信号通路整合的，该信号通路控制细胞迁移的模式。在这篇评论中，我们提出 3D 细胞迁移的模式受涉及细胞-基质黏附、RhoA 信号和肌动球蛋白收缩性的信号轴的控制，这可能代表控制 3D 细胞迁移的普遍机制。
