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|Pharmacological impairment of s-nitrosoglutathione or thioredoxin reductases augments protein S-Nitrosation in human hepatocarcinoma cells|
|Authors: ||Lopez-Sanchez, L.M. (Laura M.)|
Corrales, F.J. (Fernando José)
Lopez-Pedrera, C. (Chary)
Aranda, E. (E)
Rodriguez-Ariza, A. (Antonio)
Plicamycin/analogs & derivatives
Thioredoxin-Disulfide Reductase/antagonists & inhibitors
|Issue Date: ||2010|
|Publisher: ||International Institute of Anticancer Research|
|Publisher version: ||http://ar.iiarjournals.org/content/30/2/415|
|Citation: ||Lopez-Sanchez LM, Corrales FJ, Lopez-Pedrera C, Aranda E, Rodriguez-Ariza A. Pharmacological impairment of s-nitrosoglutathione or thioredoxin reductases augments protein S-Nitrosation in human hepatocarcinoma cells. Anticancer Res 2010 Feb;30(2):415-421.|
S-Nitrosoglutathione reductase (GSNOR) and thioredoxin enzyme systems participate in cellular defence against nitrosative stress. Pharmacological interventions against these enzyme systems might represent valuable strategies to impair S-nitrosothiol (SNO) homeostasis in tumour cells.
MATERIALS AND METHODS:
Human HepG2 cells were pre-treated with mithramycin A or auranofin and exposed to S-nitroso-L-cysteine. GSNOR mRNA levels were analyzed by quantitative real-time reverse transcriptase-polymerase chain reaction and S-nitrosated proteins were detected and purified using the biotin-switch approach. Proteins were identified using electrospray ionization tandem mass spectrometry.
Mithramycin interfered with GSNOR induction resulting in an increased cellular sensitivity to protein S-nitrosation. Moreover, the thioredoxin reductase inhibitor auranofin also increased cellular susceptibility to S-nitrosoprotein formation. The impairment of these two cellular defense systems against nitrosative stress resulted in different sets of S-nitrosated proteins, as revealed by the proteomics approach.
Our results suggest that pharmacological intervention with mithramycin or auranofin may constitute promising tools for altering SNO homeostasis in tumour cells.
|Permanent link: ||http://hdl.handle.net/10171/21474|
|Appears in Collections:||DA - CIMA - Unidad de Proteómica, Genómica y Bioinformática - Artículos de revista|
DA - CIMA - Terapia génica y Hepatología - Hepatología bioquímica - Artículos de revista
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