Abstract
We have identified a novel gene inducible by wild-type p53. A significant correlation between expression of this gene and p53 status in cells derived from esophageal cancers indicated that this gene is likely to be specifically regulated in a p53-dependent manner. As the predicted amino acid sequence showed a high degree of homology to the family of glycosyl-phosphatidylinositol (GPI)-anchored membrane proteins, we termed this gene GML (GPI-anchored molecule-like protein). Introduction of GML cDNA suppressed the growth of esophageal cancer cells in culture. A correlation between the presence of GML expression and the sensitivity of esophageal cancer cells to anti-cancer drugs implied that the gene product plays a significant role in the apoptotic pathway or cell-cycle regulation induced by p53 after DNA damage.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Antibiotics, Antineoplastic / pharmacology
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Bleomycin / pharmacology
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Cell Cycle Proteins*
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Cloning, Molecular
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Colonic Neoplasms / genetics
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Colonic Neoplasms / metabolism
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Colony-Forming Units Assay
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Drug Resistance, Neoplasm / genetics*
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Esophageal Neoplasms / drug therapy
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Esophageal Neoplasms / genetics
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GPI-Linked Proteins
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Gene Expression Regulation, Neoplastic
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Genes, p53*
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Glycosylphosphatidylinositols / metabolism*
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Humans
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Membrane Proteins / genetics*
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Membrane Proteins / isolation & purification
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Membrane Proteins / metabolism*
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Molecular Sequence Data
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Neoplasm Proteins*
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Sequence Analysis, DNA
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Sequence Homology, Amino Acid
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Tumor Cells, Cultured
Substances
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Antibiotics, Antineoplastic
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Cell Cycle Proteins
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GML protein, human
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GPI-Linked Proteins
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Glycosylphosphatidylinositols
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Membrane Proteins
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Neoplasm Proteins
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Bleomycin
Associated data
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GENBANK/AB000381
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GENBANK/D64137
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GENBANK/D84290