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

被引:0
|
作者
Q. D. Campbell Hewson
P. E. Lovat
M. Corazzari
J. B. Catterall
C. P. F. Redfern
机构
[1] University of Newcastle upon Tyne,Northern Institute for Cancer Research and School of Clinical Medical Sciences
[2] INMI-IRCCS Lazzaro Spallanzani,Northern Institute for Cancer Research, Medical School
[3] University of Newcastle,undefined
来源
Apoptosis | 2005年 / 10卷
关键词
apoptosis; fenretinide; neuroblastoma; NF-κ B; retinoic acid;
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学科分类号
摘要
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
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页码:493 / 498
页数:5
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