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Sodium butyrate inhibits expression of urokinase and its receptor mRNAs at both transcription and post-transcription levels in colon cancer cells.

作者信息

Dang J, Wang Y, Doe W F

机构信息

Division of Clinical Sciences, John Curtin School of Medical Research, Australian National University, Camberra.

出版信息

FEBS Lett. 1995 Feb 13;359(2-3):147-50. doi: 10.1016/0014-5793(95)00029-9.

Abstract

The effects of butyrate on the modulation of urokinase plasminogen activator (uPA) and its receptor (uPAR) mRNAs were studied. While both mRNA levels were increased after stimulation by tumor necrosis factor alpha (TNF alpha), phorbol ester (PMA) and cycloheximide, they were inhibited by butyrate at 2.5 to 25 mM. Nuclear run-on transcription assays indicated that uPA mRNA was modulated by butyrate at the transcriptional level but the uPAR gene was regulated at both transcriptional and post-transcriptional levels in the presence or absence of TNF alpha. In the presence of PMA, however, butyrate acts at the post-transcriptional level on both genes.

摘要

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