Endoplasmic reticulum calcium release potentiates the ER stress and cell death caused by an oxidative stress in MCF-7 cells

Abstract

Please cite this article as: Dejeans N, Tajeddine N, Beck R, Verrax J, Taper H, Gailly P, Calderon PB, Endoplasmic reticulum calcium release potentiates the ER stress and cell death caused by an oxidative stress in MCF-7 cells, Biochemical Pharmacology (2008), doi:10.1016/j.bcp.2009 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 2 ABSTRACTIncrease in cytosolic calcium concentration ([Ca 2+ ] c ), release of endoplasmic reticulum (ER) calcium ([Ca 2+ ] er ) and ER stress have been proposed to be involved in oxidative toxicity.Nevertheless, their relative involvements in the processes leading to cell death are not well defined. In this study, we investigated whether oxidative stress generated during ascorbatedriven menadione redox cycling (Asc/Men) could trigger these three events, and, if so, A c c e p t e d M a n u s c r i p t 3 IntroductionIt has long been known that disruption of intracellular calcium homeostasis is one of the primary processes in the early development of cell injury [1][2][3] [19,[24][25][26][27][28]. In summary, ER homeostasis is a fragile equilibrium, which can be modulated by dysregulation of calcium or oxidative/reductive balance, features previously associated with oxidative stress. However, studies of the links between these factors are scarce.We and others have shown that the association of ascorbate and menadione is an H 2 O 2 -generating system that results in necrosis-like cell death in a wide variety of cancer cell types [29][30][31][32][33][34][35] including MCF-7 cells (a human breast derived cell line), and that loss of calcium homeostasis appeared to be a major factor in the cytotoxicity [36]. The aim of the present study was to investigate the role of disruption of calcium homeostasis and a potential involvement of ER stress in the mechanisms leading to cancer cell death from an oxidative Materials and methods ChemicalsMenadione sodium bisulfite (Men), sodium ascorbate ( Cell Culture and TreatmentsThe MCF-7 cell line was a gift from Dr. F. Brasseur (Ludwig Institute for Cancer Research, LICR-Brussels). The cells were cultured in DMEM (Dulbecco's modified eagle medium, (Gibco BRL, Life Technologies, Merelbeke, BE)) supplemented with 10% fetal calf serum, penicillin (10 000 U/ml), streptomycin (10 mg/ml) and 1.2% glutamine. The cultures were maintained at a density of about 50x10³ cells/cm². The medium was changed at 48-72 h intervals. All cultures were maintained at 37°C in 95% air/5% CO2 with 100% humidity. minutes before the addition of ascorbate and menadione. Cells were incubated with TG or iodoacetate at concentration...

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