Nucleating actin for invasion

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Abstract
Actin polymerization inside cells is initiated by actin nucleation factors. Reassembly of the actin cytoskeleton is essential for invasive cell migration. Understanding the specific mechanisms of action and regulation of the diverse and growing number of actin nucleators is likely to provide new ideas for developing treatments that inhibit cancer spread and inflammatory conditions. Actin nucleators such as formins or the Arp2/3 complex and nucleation-promoting factors have numerous and diverse functions in invasive cancer cell migration, including the formation of protrusive structures, assembly of cell–cell contacts and matrix degradation. In addition, they have been implicated in the regulation of proinvasive signalling pathways. There is now a large body of clinical evidence for specific roles of actin nucleators in cancer progression. Importantly, many of these factors seem to be associated with advanced disease and the metastatic spread of human cancers. Actin nucleation factors now emerge as promising targets for therapeutic intervention in metastatic and invasive or inflammatory diseases. The first small-molecule inhibitors of actin nucleators have been reported very recently.

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