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Significance Cell motility plays important roles in normal physiology and numerous disease states, including cancers. Cofilin, a key player in cell locomotion, controls the direction and the force of cell protrusion. Our study establishes the cofilin phosphatase chronophin (CIN) as a major component of a PI3-kinase–mediated, Rac1-dependent signaling mechanism that activates cofilin downstream of EGF receptor in mammary carcinoma cells. During EGF stimulation, CIN redistributes to the cell edge, where it regulates cofilin-dependent actin turnover and coordinates cell protrusion and retraction dynamics. Our data uncover previously unidentified molecular mechanisms regulating cofilin in time and space in tumor cells and expand our understanding of cancer cell movement, a critical step in the process of metastasis.

Chronophin coordinates cell leading edge dynamics by controlling active cofilin levels