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The NF-κB pathway mediates fenretinide-induced apoptosis in SH-SY5Y neuroblastoma cells

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.

Publication metadata

Author(s): Campbell-Hewson, Q., Lovat, P.E., Corazzari, M., Catterall, J.B., Redfern, C.P.F.

Publication type: Article

Publication status: Published

Journal: Apoptosis

Year: 2005

Volume: 10

Issue: 3

Pages: 493-498

Print publication date: 01/05/2005

ISSN (print): 1360-8185

ISSN (electronic): 1573-675X


DOI: 10.1007/s10495-005-1878-z

PubMed id: 15909111


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