Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/62093
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Type: Journal article
Title: Targeting GRP78 to enhance melanoma cell death
Author: Martin, S.
Hill, D.
Paton, J.
Paton, A.
Birch-Machin, M.
Lovat, P.
Redfern, C.
Citation: Pigment Cell and Melanoma Research, 2010; 23(5):675-682
Publisher: Wiley-Blackwell Publishing
Issue Date: 2010
ISSN: 1755-1471
1755-148X
Statement of
Responsibility: 
Shaun Martin, David S. Hill, James C. Paton, Adrienne W. Paton, Mark A. Birch-Machin, Penny E. Lovat, Chris P.F. Redfern
Abstract: Targeting endoplasmic reticulum stress-induced apoptosis may offer an alternative therapeutic strategy for metastatic melanoma. Fenretinide and bortezomib induce apoptosis of melanoma cells but their efficacy may be hindered by the unfolded protein response, which promotes survival by ameliorating endoplasmic reticulum stress. The aim of this study was to test the hypothesis that inhibition of GRP78, a vital unfolded protein response mediator, increases cell death in combination with endoplasmic reticulum stress-inducing agents. Down-regulation of GRP78 by small-interfering RNA increased fenretinide- or bortezomib-induced apoptosis. Treatment of cells with a GRP78-specific subtilase toxin produced a synergistic enhancement with fenretinide or bortezomib. These data suggest that combining endoplasmic reticulum stress-inducing agents with strategies to down-regulate GRP78, or other components of the unfolded protein response, may represent a novel therapeutic approach for metastatic melanoma.
Keywords: melanoma
glucose-regulated protein 78
endoplasmic reticulum stress
fenretinide
bortezomib
Rights: © 2010 John Wiley & Sons A/S
DOI: 10.1111/j.1755-148X.2010.00731.x
Published version: http://dx.doi.org/10.1111/j.1755-148x.2010.00731.x
Appears in Collections:Aurora harvest 5
Molecular and Biomedical Science publications

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