Abstract

The RAS - Extracellular signal-regulated kinase (RAS-ERK) pathway plays a conserved role in promoting cell migration and invasion. Growth factors, adhesion, and oncogenes activate ERK. While historically studied with respect to its control of cell proliferation and differentiation, the signaling pattern and effectors specific for cell migration are now coming to light. New advances in pathway probes have revealed how steady-state ERK activity fluctuates within individual cells and propagates to neighboring cells. We review new findings on the different modes of ERK pathway stimulation and how an increased baseline level of activity promotes single cell and collective migration and invasion. We discuss how ERK drives actin polymerization and adhesion turnover for edge protrusion and how cell contraction stimulates cell movement and ERK activity waves in epithelial sheets. With the steady development of new biosensors for monitoring spatial and temporal ERK activity, determining how cells individually interpret the multiple in vivo signals to ERK is within reach.

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