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Human urokinase receptor expression is inhibited by amiloride and induced by tumor necrosis factor and phorbol ester in colon cancer cells
Author(s) -
Wang Yao,
Jones Caroline J.,
Dang Jinjun,
Liang Xiaoming,
Olsen Jane E.,
Doe William F.
Publication year - 1994
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(94)01032-3
Subject(s) - urokinase receptor , amiloride , tumor necrosis factor alpha , microbiology and biotechnology , receptor , signal transduction , chemistry , activator (genetics) , phorbol , cancer research , gene expression , messenger rna , plasminogen activator , endocrinology , biology , medicine , gene , biochemistry , protein kinase c , sodium , organic chemistry
The modulation of urokinase plasminogen activator receptor (uPAR) gene expression by tumor necrosis factor alpha (TNFα), phorbol ester (PMA) and amiloride was studied in three colon cancer cell lines. uPAR mRNA and protein were induced by TNFα and by PMA but were inhibited by amiloride at concentrations of 0.1 to 1 mM in the presence or absence of TNFα and PMA. Nuclear run‐on transcription assay indicated that the effects of amiloride and TNFα were mediated at least in part at the transcriptional level, whereas PMA may act in part via a post‐transcriptional mechanism. These results suggested that uPAR gene expression is modulated by multiple signal transduction pathways.