"Cell movement is the basic recipe of life, and all cells have the capacity to move," says Roberto Dominguez, Ph.D., professor of Physiology at the Perelman School of Medicine, University of Pennsylvania. Motility – albeit on a cellular spatial scale -- is necessary for wound healing, clotting, fetal development, nerve connections, and the immune response, among other functions. On the other hand, cell movement can be deleterious when cancer cells break away from tumors and migrate to set up shop in other tissues during cancer metastasis. The Dominguez team, with postdoctoral fellow David Kast, Ph.D., and colleagues, reported online ahead of print on Marh 2, 2014 in Nature Structural & Molecular Biology how a key cell-movement protein called IRSp53 is regulated in a resting and active state, and what this means for cancer-cell metastasis. "We characterized how IRSp53 connects to the cell-motility machinery," says Dr. Kast. "It does this by starting the formation of cell filopodia - extensions that form when a cell needs to move." "Cells move like an inchworm," explains Dr. Dominguez. "Filopodia are at the leading edge of moving cells." The trailing end of the cell follows the move forward through contraction of actin and myosin in the cytoskeleton, much like muscle contraction. A cell pushes out the leading edge of its membrane, and sticks it down on whatever it is moving across, namely other cells, and then moves the cell body along, unsticking the back end. This sets the cell up for its next move. IRSp53 contains a region called a BAR domain that binds to and shapes cell membranes. Other parts of the protein connect it to the cytoskeleton (internal bits that give a cell structure and shape). Together, through the binding of cell membranes and other proteins IRSp53 regulates cell movement.
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