Abstract
Cell migration is a crucial event for tissue organization during development, and its dysregulation leads to several diseases, including cancer. Cells exhibit various types of migration, such as single mesenchymal or amoeboid migration, collective migration and scaffold cell-dependent migration. The migration properties are partly dictated by cell adhesion and its endocytic regulation. While an epithelial-mesenchymal transition (EMT)-mediated mesenchymal cell migration requires the endocytic recycling of integrin-mediated adhesions after the disruption of cell-cell adhesions, an amoeboid migration is not dependent on any adhesions to extracellular matrix (ECM) or neighboring cells. In contrast, a collective migration is mediated by both cell-cell and cell-ECM adhesions, and a scaffold cell-dependent migration is regulated by the endocytosis and recycling of cell-cell adhesion molecules. Although some invasive carcinoma cells exhibit an EMT-mediated mesenchymal or amoeboid migration, other cancer cells are known to maintain cadherin-based cell-cell adhesions and epithelial morphology during metastasis. On the other hand, a scaffold cell-dependent migration is mainly utilized by migrating neurons in normal developing brains. This review will summarize the structures of cell adhesions, including adherens junctions and focal adhesions, and discuss the regulatory mechanisms for the dynamic behavior of cell adhesions by endocytic pathways in cell migration in physiological and pathological conditions, focusing particularly on neural development and cancer metastasis.
Highlights
Cell adhesion is essential for the organization and various biological functions of multicellular organisms
While phosphatidylinositol 3-kinase (PI3K) and Akt regulate the trafficking of αvβ3- and α5β1-integrins from Rab11-positive recycling endosomes to the plasma membranes, platelet-derived growth factor (PDGF) treatment promotes the
The metastasis of carcinomas consists of several steps [73,110] (Figure 5). (i) Following the formation of a primary tumor, some tumor cells detach from the primary tumor; (ii) These tumor cells invade the basement membranes and local mesenchymal tissues; (iii) They undergo transendothelial migration into blood or lymphatic vessels; (iv) Escaping from the immune system, they survive in the circulation; (v) The cancer cells attach to the vessel wall in the distant organ and migrate out of the vessel; (vi) They proliferate to establish colonies at the secondary sites
Summary
Cell adhesion is essential for the organization and various biological functions of multicellular organisms. There are two major types of cell adhesions; cell-to-cell and cell-to-extracellular matrix (ECM), both of which consist of transmembrane cell adhesion molecules, intracellular scaffold or signaling proteins and cytoskeletons (Figure 1). The major transmembrane proteins at cell-ECM adhesions are integrin heterodimers [2]. These cell-cell and cell-ECM adhesion complexes are stabilized by actin cytoskeleton or intermediate filaments, but dynamically rearranged under some circumstances, such as cell migration and cancer metastasis [3,4]. Recent reports indicate that some cancer cells maintain cell-cell adhesions and epithelial morphology during metastasis This type of migration, called a collective cell migration, requires both cell-cell and cell-ECM adhesions. I introduce the physiological and pathological roles of the regulation of cell adhesions in various types of cell migration in neural development and cancer metastasis
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