5.2. Therapeutic targeting strategies
Targeting key proteins involved in the regulation of lamellipodia and filopodia dynamics presents a promising avenue for therapeutic intervention. Small molecules and inhibitors designed to disrupt the formation or activity of these cellular protrusions have the potential to impede cancer cell invasion. Small molecules targeting Rho GTPases, such as Rac1 and Cdc42, can interfere with the signaling pathways responsible for lamellipodia and filopodia formation (Table 1 ). These inhibitors aim to disrupt the cytoskeletal dynamics, inhibiting the protrusive forces driving cancer cell migration [59–61]. Meanwhile, targeting the WASP-Arp2/3 complex pathway with specific inhibitors can disrupt the nucleation and branching of actin filaments, inhibiting lamellipodia formation. Such inhibitors may attenuate the invasive potential of cancer cells [45]. Therapeutic strategies can also be designed to target signaling pathways that regulate lamellipodia and filopodia dynamics. By modulating these pathways, it is possible to influence the migratory behavior of cancer cells and impede their invasive capabilities. Small molecules targeting integrins or FAK can disrupt the signaling cascades that link extracellular signals to the actin cytoskeleton. This interference may hinder the formation and stability of lamellipodia and filopodia [62–64]. Developing inhibitors specific to Ena/VASP proteins could hinder the bundling and elongation of actin filaments in filopodia. This approach may prove effective in curtailing the formation and function of filopodia in cancer cells [65]. Tailoring therapeutic strategies to interfere with the molecular machinery governing lamellipodia and filopodia dynamics represents a novel approach in cancer treatment, particularly for malignancies with a strong invasive component.