Cell migration is essential to many physiological processes; however, it is also a cause of cancer metastasis formation and other pathological phenomena. Due to structural and functional variety of cells, a variety of structures formed by the cell membrane, which are designed to initiate or maintain cell movement, are observed. The work describes 12 such structures: lamellipodium, lamellum, filopodium, microspikes, blebs, lobopodium, invadopodium, podosomes, dorsal and peripheral ruffles, pseudopodium and uropodium. We described a characteristics of the structure, mechanism of its formation and occurrence. The key structural protein of almost all of these structures is actin, its polymerization pushes the cell membrane in the direction of movement. Formation of a specific protrusion depends on the actin binding proteins which regulate the process of G actin association to the filaments. For example, Arp2/3 determines
the formation of branched filaments, which results in the formation of wide, flat lamellipodium,
and fascin enables the formation of long bundles, which results in filopodia formation.
On the other hand, there is also an actin-independent way of movement, called amoeboid, in
which myosin plays a central role and on the cell surface appear vesicular structures called
blebs. Some structures are associated with proteolytic activity, particularly invadopodia and
podosomes, through which the cells can degrade extracellular matrix and penetrate deeper
into the tissues. These structures not only allow the extension of the cell body to enable migration,
but they can also be involved in the environment perception, serve as mechanosensors
and interact with other cells. The control of the formation of protrusive structures is of great
importance in oncology, immunology and cardiovascular medicine.
Connexin43 controls N-cadherin transcription during collective cell migration
