Abstract
RELN (Reelin) is an extracellular glycoprotein that plays a critical role in neuronal migration. Here we show that the RELN gene is frequently silenced in gastric cancers (GCs) by aberrant promoter hypermethylation. Although RELN was strongly expressed in non-tumor gastric epithelia, its expression was weak, or absent, in GC cell lines and primary GC tumors. Absence of RELN expression significantly correlated with a more advanced stage of GC. Methylation of the RELN promoter was frequently found in GC cell lines and in primary GC tumors. These findings suggest that disruption of the RELN pathway may be involved in gastric carcinogenesis.
MeSH terms
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Aged
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Cell Adhesion Molecules, Neuronal / biosynthesis*
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Cell Adhesion Molecules, Neuronal / genetics*
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Cell Line, Tumor
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Cell Movement
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DNA Methylation
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DNA Primers / genetics
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Epigenesis, Genetic*
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Epithelium / metabolism
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Extracellular Matrix Proteins / biosynthesis*
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Extracellular Matrix Proteins / genetics*
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Female
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Humans
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Male
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Middle Aged
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Models, Genetic
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Nerve Tissue Proteins / biosynthesis*
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Nerve Tissue Proteins / genetics*
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Neurons / metabolism*
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Promoter Regions, Genetic
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RNA, Messenger / metabolism
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Reelin Protein
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Reverse Transcriptase Polymerase Chain Reaction
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Serine Endopeptidases / biosynthesis*
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Serine Endopeptidases / genetics*
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Stomach Neoplasms / genetics*
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Stomach Neoplasms / metabolism*
Substances
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Cell Adhesion Molecules, Neuronal
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DNA Primers
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Extracellular Matrix Proteins
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Nerve Tissue Proteins
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RNA, Messenger
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Reelin Protein
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RELN protein, human
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Serine Endopeptidases