Mesenchymal Migration as a Therapeutic Target in Glioblastoma

Figure 2

Schematic representation of a glioblastoma cell migrating through a 3D ECM. During migration, the cell becomes polarized with respect to the direction of movement into a leading and a trailing edge. The leading edge is characterized by dynamic membrane rearrangements and proteolytic breakdown of ECM, enabling the cell to protrude at its front. The trailing edge displays constant disassembly of mature focal adhesions, therefore promoting dislodgement of the rear. Tight regulation of actin assembly and disassembly is crucial for migration, controlling cellular protrusion, as well as myosin II-mediated contraction in interplay with myosin II.