Fig. 4: Cancer cell migration and invasion through specialized protrusions and cytoskeletal reorganization.

a Epithelial cells have strong cell-to-cell adhesion through adherens junctions and hemidesmosomes. The EMT transcription factors suppress the expression of epithelial cell markers such as E-cadherin and cytokeratin and induce the expression of mesenchymal cell marker such as vimentin during the EMT process. b The invadopodia promote cell invasion by increasing ECM degradation via MMPs, which are anchored to the plasma membrane by binding to integrins via talin and vinculin. The ROCK2–LIMK pathway regulates the stability of invadopodia by inhibiting cofilin. CLASP1 and SLAIN2 promote the microtubule growth. Plectin reinforces invadopodia stability by linking intermediate filaments to actin filaments. c The leader bleb is formed owing to increased pressure from actomyosin contraction at the back of the cell, driving the cell migration. d The lamellipodia enhance the cell motility through actin polymerization, mediated by Ena/VASP interacting with lamellipodin. e The myosin II contraction of stress fibers at the posterior of mesenchymal cells induces focal adhesion disassembly and cell migration. f The filopodia recognize the extracellular environment by binding to integrins via myosin-X. ROCK2, rho-associated coiled-coil protein kinase 2.