During development of metastasis, tumor cells migrate through different tissues and encounter different extracellular matrices. An ability of cells to adapt mechanisms of their migration to these diverse environmental conditions, called migration plasticity, gives tumor cells an advantage over normal cells for long distant dissemination. Different modes of individual cell motility—mesenchymal and amoeboid—are driven by different molecular mechanisms, which largely depend on functions of the actin cytoskeleton that can be modulated in a wide range by cellular signaling mechanisms in response to environmental conditions. Various triggers can switch one motility mode to another, but regulations of these transitions are incompletely understood. However, understanding of the mechanisms driving migration plasticity is instrumental for finding anti-cancer treatment capable to stop cancer metastasis. In this review, we discuss cytoskeletal features, which allow the individually migrating cells to switch between mesenchymal and amoeboid migrating modes, called mesenchymal-to-amoeboid transition (MAT). We briefly describe main characteristics of different cell migration modes, and then discuss the triggering factors that initiate MAT with special attention to cytoskeletal features essential for migration plasticity.

在转移的发展过程中，肿瘤细胞通过不同的组织迁移并遇到不同的细胞外基质。细胞使其迁移机制适应这些不同环境条件的能力，称为迁移可塑性，使肿瘤细胞比正常细胞具有远距离传播的优势。个体细胞运动的不同模式——间充质和变形虫——是由不同的分子机制驱动的，这在很大程度上取决于肌动蛋白细胞骨架的功能，可以通过细胞信号机制响应环境条件在大范围内调节肌动蛋白细胞骨架。各种触发器可以将一种运动模式切换到另一种，但这些转换的规则尚不完全清楚。然而，了解驱动迁移可塑性的机制有助于找到能够阻止癌症转移的抗癌治疗。在这篇综述中，我们讨论了细胞骨架特征，这些特征允许单独迁移的细胞在间充质和变形虫迁移模式之间切换，称为间充质到变形虫转换 (MAT)。我们简要描述了不同细胞迁移模式的主要特征，然后讨论了启动 MAT 的触发因素，特别关注迁移可塑性所必需的细胞骨架特征。