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Lookup NU author(s): Dr Quentin Campbell Hewson,
Professor Penny Lovat,
Dr Jonathan Catterall,
Dr Chris RedfernORCiD
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Fenretinide induces apoptosis in SH-SY5Y neuroblastoma cells via a signaling pathway involving the production of reactive oxygen species (ROS), 12-lipoxygenase activity and the induction of the GADD153 transcription factor. NF-κ B is a key element of many cell signaling pathways and adopts a pro- or anti-apoptotic role in different cell types. Studies have suggested that NF-κ B may play a pro-apoptotic role in SH-SY5Y cells, and in other cell types NF-κ B activation may be linked to lipoxygenase activity. The aim of this study was to test the hypothesis that NF-κ B activity mediates fenretinide-induced apoptosis in SH-SY5Y neuroblastoma cells. Using a dominant-negative construct for Iκ Bα stably transfected into SH-SY5Y cells, we show that apoptosis, but not the induction of ROS, in response to fenretinide was blocked by abrogation of NF-κ B activity. In parental SH-SY5Y cells, fenretinide induced NF-κ B activity and Iκ Bα phosphorylation. These results suggest that NF-κ B activity links fenretinide-induced ROS to the induction of apoptosis in SH-SH5Y cells, and may be a target for the future development of drugs for neuroblastoma therapy. © 2005 Springer Science + Business Media, Inc.
Author(s): Campbell-Hewson, Q., Lovat, P.E., Corazzari, M., Catterall, J.B., Redfern, C.P.F.
Publication type: Article
Publication status: Published
Print publication date: 01/05/2005
ISSN (print): 1360-8185
ISSN (electronic): 1573-675X
PubMed id: 15909111
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