Abstract
Galectin-1 has been demonstrated to be a mediator of T-cell apoptosis acting on activated T-cells and, in a selective manner, on different T leukemia cell lines. Here we show that the sensitivity to galectin-1 is associated with repression of the endogenous galectin-1 gene whereas non-sensitive cells express high levels of galectin-1. Repression of galectin-1 gene in sensitive cells is associated with hyper-methylation of the promoter region. Transient treatment of non-expressing cells with the demethylating agent 5-azacytidine led to irreversible demethylation and subsequent reactivation of galectin-1 gene.
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 / pharmacology
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DNA (Cytosine-5-)-Methyltransferases / antagonists & inhibitors
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DNA (Cytosine-5-)-Methyltransferases / metabolism
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DNA Methylation* / drug effects
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Enzyme Inhibitors / pharmacology
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Galectin 1
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Gene Expression Regulation, Leukemic* / drug effects
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Hemagglutinins / biosynthesis
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Hemagglutinins / genetics*
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Humans
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Leukemia, T-Cell / genetics
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Leukemia, T-Cell / metabolism
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Leukemia, T-Cell / pathology*
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Neoplasm Proteins / antagonists & inhibitors
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Neoplasm Proteins / biosynthesis
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Neoplasm Proteins / genetics*
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Promoter Regions, Genetic
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Tumor Cells, Cultured / drug effects
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Tumor Cells, Cultured / metabolism
Substances
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Antimetabolites, Antineoplastic
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Enzyme Inhibitors
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Galectin 1
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Hemagglutinins
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Neoplasm Proteins
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DNA (Cytosine-5-)-Methyltransferases
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Azacitidine