Wang Y, Jones C J, Dang J, Liang X, Olsen J E, Doe W F
Division of Clinical Sciences, John Curtin School of Medical Research, Australian National University, Canberra.
FEBS Lett. 1994 Oct 17;353(2):138-42. doi: 10.1016/0014-5793(94)01032-3.
The modulation of urokinase plasminogen activator receptor (uPAR) gene expression by tumor necrosis factor alpha (TNF alpha), phorbol ester (PMA) and amiloride was studied in three colon cancer cell lines. uPAR mRNA and protein were induced by TNF alpha and by PMA but were inhibited by amiloride at concentrations of 0.1 to 1 mM in the presence or absence of TNF alpha and PMA. Nuclear run-on transcription assay indicated that the effects of amiloride and TNF alpha were mediated at least in part at the transcriptional level, whereas PMA may act in part via a posttranscriptional mechanism. These results suggested that uPAR gene expression is modulated by multiple signal transduction pathways.
在三种结肠癌细胞系中研究了肿瘤坏死因子α（TNFα）、佛波酯（PMA）和氨氯吡咪对尿激酶型纤溶酶原激活物受体（uPAR）基因表达的调节作用。uPAR mRNA和蛋白在有或无TNFα和PMA的情况下，均可被TNFα和PMA诱导，但在0.1至1 mM浓度的氨氯吡咪作用下受到抑制。核转录活性分析表明，氨氯吡咪和TNFα的作用至少部分是在转录水平介导的，而PMA可能部分通过转录后机制发挥作用。这些结果提示uPAR基因表达受多种信号转导途径的调节。
