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• W2146278300 abstract "Metastasis is a leading cause of mortality and morbidity in cancer. Urokinase (uPA), only expressed by the highly invasive cancer cells, has been implicated in invasion, metastases, and angiogenesis of several malignancies including breast cancer. Because uPA expression is strongly correlated with its hypomethylated state, we utilized the uPA gene in the highly invasive MDA-231 human breast cancer cells as a model system to test the hypothesis that pharmacological reversal of the uPA promoter hypomethylation would result in its silencing and inhibition of metastasis. <i>S</i>-Adenosyl-l-methionine (AdoMet) has previously been shown to cause hypermethylation and inhibit demethylation. Treatment of MDA-231 cells with AdoMet, but not its unmethylated analogue <i>S</i>-adenosylhomocysteine, significantly inhibits uPA expression and tumor cell invasion <i>in vitro</i> and tumor growth and metastasis <i>in vivo</i>. The effects of AdoMet on uPA expression were reversed by the demethylating agent 5′-azacytidine, supporting the conclusion that AdoMet effects are caused by hypermethylation. Knockdown of the methyl-binding protein 2 also causes a significant inhibition of uPA expression <i>in vitro</i> and tumor growth and metastasis <i>in vivo</i>. These treatments did not have any effects on estrogen receptor expression, suggesting that inhibition of hypomethylation will not affect genes already silenced by hypermethylation. These data are consistent with the hypothesis that hypomethylation of critical genes like uPA plays a causal role in metastasis. Inhibition of hypomethylation can thus be used as a novel therapeutic approach to silence the pro-metastatic gene uPA and block breast cancer progression into the aggressive and metastatic stages of the disease." @default.
• W2146278300 created "2016-06-24" @default.
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• W2146278300 date "2004-07-01" @default.
• W2146278300 modified "2023-10-11" @default.
• W2146278300 title "Reversal of the Hypomethylation Status of Urokinase (uPA) Promoter Blocks Breast Cancer Growth and Metastasis" @default.
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• W2146278300 doi "https://doi.org/10.1074/jbc.m401669200" @default.
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