Abstract
Through a genome-wide cDNA microarray, we identified that the paternally expressed gene 10 (PEG10) was highly expressed in a great majority of hepatocellular carcinomas, although its expression was absent in normal liver cells. Exogenous expression of PEG10 conferred oncogenic activity and transfection of hepatoma cells with antisense S-oligonucleotides suppressing PEG10 resulted in their growth inhibition. Additional experiments revealed that PEG10 protein associated with SIAH1, a mediator of apoptosis, and that overexpression of PEG10 decreased the cell death mediated by SIAH1. These findings suggested that development of drug(s) inhibiting PEG10 activity could be a novel approach for the treatment of hepatocellular carcinomas.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / physiology*
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Apoptosis Regulatory Proteins
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Carcinoma, Hepatocellular / etiology*
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Carcinoma, Hepatocellular / metabolism
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Cell Division
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Cell Line
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Cell Transformation, Neoplastic
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DNA-Binding Proteins
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Gene Expression Regulation, Neoplastic
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Humans
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Kidney
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Liver Neoplasms / etiology*
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Liver Neoplasms / metabolism
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Neoplasm Proteins / biosynthesis
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Neoplasm Proteins / genetics
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Nuclear Proteins / genetics
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Nuclear Proteins / physiology*
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Oligodeoxyribonucleotides, Antisense / pharmacology
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Protein Interaction Mapping
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Proteins / antagonists & inhibitors
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Proteins / genetics
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Proteins / physiology*
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RNA-Binding Proteins
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Recombinant Fusion Proteins / physiology
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Transfection
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Tumor Cells, Cultured
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Tumor Stem Cell Assay
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Ubiquitin-Protein Ligases
Substances
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Apoptosis Regulatory Proteins
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DNA-Binding Proteins
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Neoplasm Proteins
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Nuclear Proteins
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Oligodeoxyribonucleotides, Antisense
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PEG10 protein, human
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Proteins
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RNA-Binding Proteins
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Recombinant Fusion Proteins
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Ubiquitin-Protein Ligases
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seven in absentia proteins