{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T12:50:34Z","timestamp":1772801434196,"version":"3.50.1"},"reference-count":35,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,3,1]],"date-time":"2004-03-01T00:00:00Z","timestamp":1078099200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2004,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We have previously reported that interferon\u2010\u03b1 (IFN\u03b1) induces apoptosis and EGF can antagonize this effect in human epidermoid cancer KB cells. Since apoptosis occurs together with cytoskeleton reorganization we have evaluated if IFN\u03b1 and EGF could modulate cell remodeling in our experimental conditions. We have found that 48 h 1,000 IU\/ml IFN\u03b1 induced structural reorganization of stress fibers and membrane delocalization and partial capping of the actin severing protein gelsolin. The transfection of KB cells with both a wild type (WT) or a C\u2010terminal truncated form of gelsolin caused overexpression of the protein and an increase of both the spontaneous and IFN\u03b1\u2010induced apoptosis and cell cytoskeletal modifications. In fact, after 48 h of treatment IFN\u03b1 induced 45% of apoptotic cell death in parental cells while an approximately 80% of cell population was apoptotic in transfected cells. These effects occurred together with an increase of the expression and consequent degradation of gelsolin. Again the addition of EGF to IFN\u03b1\u2010treated transfected cells caused a recovery of the apoptosis. Notably, IFN\u03b1 and EGF did not modify the expression of other molecules associated to cytoskeleton such as focal adhesion kinase and vinculin. In the same experimental conditions IFN\u03b1 induced also gelsolin cleavage that occurred together with caspase\u20103 activation and release of cytochrome c. All these effects were antagonized by the exposure of IFN\u03b1\u2010treated KB to 10 nM EGF for the last 12 h. Moreover, the specific inhibition of caspase\u20103 with 20 \u03bcM DEVD completely abrogated apoptosis and gelsolin cleavage induced by IFN\u03b1. In conclusion, our data are the first demonstration that IFN\u03b1 can induce morphological cell changes that are peculiar of apoptosis onset through the caspase\u20103\u2010mediated cleavage of gelsolin. Furthermore, we have demonstrated that EGF is able to antagonize these effects through the inhibition of caspase\u20103 activation. J. Cell. Physiol. 201: 71\u201383, 2004. \u00a9 2004 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.20058","type":"journal-article","created":{"date-parts":[[2004,4,2]],"date-time":"2004-04-02T15:27:19Z","timestamp":1080919639000},"page":"71-83","source":"Crossref","is-referenced-by-count":34,"title":["Apoptosis induced by interferon\u2010\u03b1 and antagonized by EGF is regulated by caspase\u20103\u2010mediated cleavage of gelsolin in human epidermoid cancer 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