Abstract
Members of the suppressor of cytokine-induced signaling (SOCS) family are negative regulators of cytokine signaling pathways. By mRNA differential display, we showed that SOCS6 was frequently down-regulated in gastric cancer (GC). Our data showed that allelic loss and promoter hypermethylation may account for the major mechanisms leading to SOCS6 inactivation. Ectopic expression of SOCS6 suppressed cell growth and colony formation, in part through eliciting intrinsic apoptotic pathway, accompanied with decreased mitochondrial membrane potential. Taken together, this study provides molecular and functional data supporting the importance of loss-of-function of SOCS6 as a frequent event in gastric tumorigenesis.
Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenocarcinoma / genetics
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Adenocarcinoma / metabolism*
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Adenocarcinoma / pathology
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Aged
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Apoptosis
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Cell Line, Tumor
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Cell Proliferation*
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DNA Methylation
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Down-Regulation
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Female
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Gene Expression Regulation, Neoplastic
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Humans
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Loss of Heterozygosity
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Male
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Membrane Potential, Mitochondrial
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Middle Aged
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Promoter Regions, Genetic
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RNA, Messenger / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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Stomach Neoplasms / genetics
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Stomach Neoplasms / metabolism*
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Stomach Neoplasms / pathology
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Suppressor of Cytokine Signaling Proteins / genetics
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Suppressor of Cytokine Signaling Proteins / metabolism*
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Time Factors
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Transfection
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Tumor Stem Cell Assay
Substances
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RNA, Messenger
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SOCS6 protein, human
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Suppressor of Cytokine Signaling Proteins