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First published online January 21, 2009
doi: 10.1242/jcs.031146

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A common cofilin activity cycle in invasive tumor cells and inflammatory cells

¹ Department of Anatomy and Structural Biology, Gruss Lipper Center for Biophotonics, Albert Einstein College of Medicine of Yeshiva University, Bronx, NY 10461, USA
² Hubrecht Institute-KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584CT, Utrecht, The Netherlands
³ CIHR Group in Matrix Dynamics, University of Toronto, Toronto, Ontario M5S 3E2, Canada

e-mails: j.vanrheenen{at}niob.knaw.nl; condeeli{at}aecom.yu.edu; michael.glogauer{at}utoronto.ca

Summary

In many cell types, the formation of membrane protrusions and directional migration depend on the spatial and temporal regulation of the actin-binding protein cofilin. Cofilin, which is important for the regulation of actin-polymerization initiation, increases the number of actin free barbed ends through three mechanisms: its intrinsic actin-nucleation activity; binding and severing of existing actin filaments; and recycling actin monomers from old filaments to new ones through its actin-depolymerization activity. The increase in free barbed ends that is caused by cofilin initiates new actin polymerization, which can be amplified by the actin-nucleating ARP2/3 complex. Interestingly, different cell systems seem to have different mechanisms of activating cofilin. The initial activation of cofilin in mammary breast tumors is dependent on PLC, whereas cofilin activation in neutrophils is additionally dependent on dephosphorylation, which is promoted through Rac2 signaling. Although the literature seems to be confusing and inconsistent, we propose that all of the data can be explained by a single activity-cycle model. In this Opinion, we give an overview of cofilin activation in both tumor cells and inflammatory cells, and demonstrate how the differences in cofilin activation that are observed in various cell types can be explained by different starting points in this single common activity cycle.

Key words: Cofilin activation cycle, Inflammation, Metastasis

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