核受体 PPARα、LRH-1 和 SHP 对 miR-200c 的调控。
Regulation of miR-200c by nuclear receptors PPARα, LRH-1 and SHP.
机构信息
Department of Medicine, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT 84132, USA.
出版信息
Biochem Biophys Res Commun. 2011 Dec 9;416(1-2):135-9. doi: 10.1016/j.bbrc.2011.11.011. Epub 2011 Nov 11.
Abstract
We investigated regulation of miR-200c expression by nuclear receptors. Ectopic expression of miR-200c inhibited MHCC97H cell migration, which was abrogated by the synergistic effects of PPARα and LRH-1 siRNAs. The expression of miR-200c was decreased by PPARα/LRH-1 siRNAs and increased by SHP siRNAs, and overexpression of the receptors reversed the effects of their respective siRNAs. SHP siRNAs also drastically enhanced the ability of the LRH-1 agonist RJW100 to induce miR-200c and downregulate ZEB1 and ZEB2 proteins. Co-expression of PPARα and LRH-1 moderately transactivated the miR-200c promoter, which was repressed by SHP co-expression. RJW100 caused strong activation of the miR-200c promoter. This is the first report to demonstrate that miR-200c expression is controlled by nuclear receptors.
摘要
我们研究了核受体对 miR-200c 表达的调控。miR-200c 的过表达抑制了 MHCC97H 细胞的迁移，而 PPARα 和 LRH-1 siRNAs 的协同作用则消除了这种抑制作用。miR-200c 的表达被 PPARα/LRH-1 siRNAs 下调，被 SHP siRNAs 上调，而受体的过表达则逆转了各自 siRNAs 的作用。SHP siRNAs 还极大地增强了 LRH-1 激动剂 RJW100 诱导 miR-200c 和下调 ZEB1 和 ZEB2 蛋白的能力。PPARα 和 LRH-1 的共表达适度地转录激活了 miR-200c 启动子，而 SHP 的共表达则抑制了其转录激活。这是首次报道核受体控制 miR-200c 的表达。
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