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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Terapia génica y Hepatología > Hepatología bioquímica > DA - CIMA - Terapia génica y Hepatología - Hepatología bioquímica - Artículos de revista >

Proteomic analysis of human hepatoma cells expressing methionine adenosyltransferase I/III Characterization of DDX3X as a target of S-adenosylmethionine
Authors: Schröder, P.C. (Paul C.)
Fernandez-Irigoyen, J. (Joaquín)
Bigaud, E. (Emilie)
Serna, A. (Antonio)
Hernandez-Alcoceba, R. (Rubén)
Lu, S.C. (Shelly C.)
Mato, J.M. (José María)
Prieto, J. (Jesús)
Corrales, F.J. (Fernando José)
Keywords: S-adenosylmethionine
Hepatocellular carcinoma
DDX3X
2D-DIGE
Mass spectrometry
Proteomics
Issue Date: 2012
Publisher: Elsevier
Publisher version: http://www.sciencedirect.com/science/article/pii/S1874391912000267
ISSN: 1876-7737
Citation: Schroder PC, Fernandez-Irigoyen J, Bigaud E, Serna A, Renandez-Alcoceba R, Lu SC, et al. Proteomic analysis of human hepatoma cells expressing methionine adenosyltransferase I/III Characterization of DDX3X as a target of S-adenosylmethionine. J Proteomics 2012 Jan 16.
Abstract
Methionine adenosyltransferase I/III (MATI/III) synthesizes S-adenosylmethionine (SAM) in quiescent hepatocytes. Its activity is compromised in most liver diseases including liver cancer. Since SAM is a driver of hepatocytes fate we have studied the effect of re-expressing MAT1A in hepatoma Huh7 cells using proteomics. MAT1A expression leads to SAM levels close to those found in quiescent hepatocytes and induced apoptosis. Normalization of intracellular SAM induced alteration of 128 proteins identified by 2D-DIGE and gel-free methods, accounting for deregulation of central cellular functions including apoptosis, cell proliferation and survival. Human Dead-box protein 3 (DDX3X), a RNA helicase regulating RNA splicing, export, transcription and translation was down-regulated upon MAT1A expression. Our data support the regulation of DDX3X levels by SAM in a concentration and time dependent manner. Consistently, DDX3X arises as a primary target of SAM and a principal intermediate of its antitumoral effect. Based on the parallelism between SAM and DDX3X along the progression of liver disorders, and the results reported here, it is tempting to suggest that reduced SAM in the liver may lead to DDX3X up-regulation contributing to the pathogenic process and that replenishment of SAM might prove to have beneficial effects, at least in part by reducing DDX3X levels. This article is part of a Special Issue entitled: Clinical Proteomics.
Permanent link: http://hdl.handle.net/10171/21562
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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