{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T09:52:16Z","timestamp":1790070736452,"version":"4.0.1"},"reference-count":38,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2011,10,15]],"date-time":"2011-10-15T00:00:00Z","timestamp":1318636800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Cell migration is accomplished by the formation of cellular protrusions such as lamellipodia and filopodia. These protrusions result from actin filament (F\u2010actin) rearrangement at the cell cortex by WASP\/WAVE family proteins and Drosophila enabled (Ena)\/vasodilator\u2010stimulated factor proteins. However, the role of each of these actin cytoskeletal regulatory proteins in the regulation of three\u2010dimensional cell invasion remains to be clarified. We found that platelet\u2010derived growth factor (PDGF) induces invasion of MDA\u2010MB\u2010231 human breast cancer cells through invasion chamber membrane pores. This invasion was accompanied by intensive F\u2010actin accumulation at the sites of cell infiltration. After PDGF stimulation, WAVE2, N\u2010WASP, and a mammalian Ena (Mena) colocalized with F\u2010actin at the sites of cell infiltration in a phosphatidylinositol 3\u2010kinase (PI3K)\u2010dependent manner. Depletion of WAVE2, N\u2010WASP, or Mena by RNA interference (RNAi) abrogated both cell invasion and intensive F\u2010actin accumulation at the invasion site. These results indicate that by mediating intensive F\u2010actin accumulation at the sites of cell infiltration, WAVE2, N\u2010WASP, and Mena are crucial for PI3K\u2010dependent cell invasion induced by PDGF. 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