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They form in response to epidermal growth factor (EGF), and contain the usual invadopodium core proteins N\u2010WASP, Arp2\/3, cortactin, cofilin, and F\u2010actin. The study of invadopodia on glass allows for higher resolution analysis including the use of total internal reflection microscopy and analysis of their relationship to other cell motility events, in particular, lamellipodium extension and chemotaxis toward an EGF gradient. Invadopodium formation on glass requires N\u2010WASP and cortactin but not microtubules. In a gradient of EGF more invadopodia form on the side of the cells facing the source of EGF. In addition, depletion of N\u2010WASP or cortactin, which blocks invadopodium fromation, inhibits chemotaxis of cells towards EGF. This appears to be a localized defect in chemotaxis since depletion of N\u2010WASP or cortactin via siRNA had no effect on lamellipodium protrusion or barbed end generation at the lamellipodium's leading edge. Since chemotaxis to EGF by breast tumor cells is involved in metastasis, inhibiting N\u2010WASP activity in breast tumor cells might prevent metastasis of tumor cells while not affecting chemotaxis\u2010dependent innate immunity which depends on WASp function in macrophages. Cell Motil. Cytoskeleton 2009. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/cm.20361","type":"journal-article","created":{"date-parts":[[2009,4,16]],"date-time":"2009-04-16T10:30:18Z","timestamp":1239877818000},"page":"303-316","source":"Crossref","is-referenced-by-count":106,"title":["N\u2010WASP and cortactin are involved in invadopodium\u2010dependent chemotaxis to EGF in breast tumor 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