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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
Author(s) -
Dang Jinjun,
Wang Yao,
Doe William F.
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00029-9
Subject(s) - urokinase receptor , cycloheximide , butyrate , sodium butyrate , transcription (linguistics) , microbiology and biotechnology , messenger rna , gene expression , chemistry , transcriptional regulation , cancer research , plasminogen activator , biology , endocrinology , gene , biochemistry , protein biosynthesis , linguistics , philosophy , fermentation
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 (TNFα), 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 TNFα. In the presence of PMA, however, butyrate acts at the post‐transcriptional level on both genes.