Abstract
Insulin-like growth factor binding protein-3 (IGFBP-3) is postulated to be a mediator of growth suppression signals. Reduced expression of the IGFBP-3 was observed in nine out of 12 human hepatocellular carcinomas (HCC) (75%). Promoter hypermethylation of the IGFBP-3 was detected in four out of 12 HCCs (33%) although mutations were not identified. The expression of IGFBP-3 was restored by the demethylating agent 5-aza-2'-deoxycytidine in HCC cell line with promoter hypermethylation (HepG2). As IGFBP-3 functions like a tumor suppressor gene, it may be used as a therapeutic target for HCC.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antimetabolites, Antineoplastic / pharmacology
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Azacitidine / analogs & derivatives*
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Azacitidine / pharmacology
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Base Sequence
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Blotting, Northern
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Carcinoma, Hepatocellular / genetics
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Carcinoma, Hepatocellular / metabolism*
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Chromosomes, Human, Pair 7
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DNA Methylation*
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DNA, Complementary / metabolism
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Decitabine
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Humans
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Insulin-Like Growth Factor Binding Protein 3 / biosynthesis*
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Insulin-Like Growth Factor Binding Protein 3 / genetics*
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Liver Neoplasms / genetics
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Liver Neoplasms / metabolism*
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Loss of Heterozygosity
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Mannosephosphates / metabolism
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Molecular Sequence Data
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Mutation
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Oligonucleotide Array Sequence Analysis
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Polymerase Chain Reaction
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Polymorphism, Single-Stranded Conformational
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Promoter Regions, Genetic*
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RNA / metabolism
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Receptor, IGF Type 2 / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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Tumor Cells, Cultured
Substances
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Antimetabolites, Antineoplastic
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DNA, Complementary
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Insulin-Like Growth Factor Binding Protein 3
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Mannosephosphates
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Receptor, IGF Type 2
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mannose-6-phosphate
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RNA
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Decitabine
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Azacitidine