Toggle Main Menu Toggle Search

ePrints

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 Redfern

Downloads

Full text for this publication is not currently held within this repository. Alternative links are provided below where available.


Abstract

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

URL: http://dx.doi.org/10.1007/s10495-005-1878-z

DOI: 10.1007/s10495-005-1878-z

PubMed id: 15909111


Altmetrics

Altmetrics provided by Altmetric


Actions

    Link to this publication


Share