Abstract
Cell migration controls developmental processes (gastrulation and tissue patterning), tissue homeostasis (wound repair and inflammatory responses), and the pathobiology of diseases (cancer metastasis and inflammation). Understanding how cells move in physiologically relevant environments is of major importance, and the molecular machinery behind cell movement has been well studied on 2D substrates, beginning over half a century ago. Studies over the past decade have begun to reveal the mechanisms that control cell motility within 3D microenvironments – some similar to, and some highly divergent from those found in 2D. In this review we focus on migration and invasion of cells powered by actin, including formation of actin-rich protrusions at the leading edge, and the mechanisms that control nuclear movement in cells moving in a 3D matrix.
Highlights
DirecƟon of migraƟonEndocytosis and invadopodia formation [53,54,55,56]
Cell migration controls developmental processes, tissue homeostasis, and the pathobiology of diseases
The suitability of 2D plastic/glass surfaces as representative biological models has been questioned in recent years due to their incredibly high rigidity compared to any surface in vivo, and the simplicity of extracellular matrix (ECM) presentation when compared to complex fibrillar interstitial matrix, for example, the connective tissue of vertebrates
Summary
Endocytosis and invadopodia formation [53,54,55,56]. In many cases the direct contribution to leading edge actin reorganisation is not known. Rac activity is clearly implicated in the migration of mesenchymal cancer cells in 3D and in vivo [35,57]. Rac knockout melanoblasts show defects in extension of pseudopodial protrusions and
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