PU.1 直接调控维甲酸诱导白血病细胞中 RIG-G 的表达。

PU.1 directly regulates retinoic acid-induced expression of RIG-G in leukemia cells.

机构信息

Department of Pathophysiology and Chemical Biology, Division of Shanghai Universities E-Institutes, Key laboratory of Cell Differentiation and Apoptosis of Minister of Education, Shanghai Jiao-Tong University School of Medicine, Shanghai, China.

出版信息

FEBS Lett. 2011 Jan 21;585(2):375-80. doi: 10.1016/j.febslet.2010.12.021. Epub 2010 Dec 19.

DOI:10.1016/j.febslet.2010.12.021

PMID:21176776

Abstract

RIG-G is a retinoic acid- or interferon-induced gene with potential anti-proliferation function. However, the mechanism underlying ATRA-induced RIG-G induction is not completely understood. Here, we demonstrate that ATRA up-regulates the expression of PU.1, which in turn directly binds to the promoter and increases the expression of RIG-G gene. Luciferase reporter assay and electrophoretic mobility shift assay reveal that PU.1 preferentially binds to one of the two putative binding sites on the RIG-G promoter. Moreover, silencing of PU.1 by shRNA markedly inhibited ATRA- but not IFNα-induced expression of RIG-G. These data provide new insight into the mechanism of ATRA-induced RIG-G expression.

摘要

RIG-G 是一种维甲酸或干扰素诱导的基因，具有潜在的抗增殖功能。然而，ATRA 诱导 RIG-G 表达的机制尚不完全清楚。在这里，我们证明 ATRA 上调了 PU.1 的表达，而 PU.1 反过来又直接结合到启动子上，增加了 RIG-G 基因的表达。荧光素酶报告基因检测和电泳迁移率变动分析揭示，PU.1 优先结合到 RIG-G 启动子上的两个假定结合位点之一。此外，shRNA 沉默 PU.1 显著抑制了 ATRA 诱导的 RIG-G 表达，但不抑制 IFNα 诱导的 RIG-G 表达。这些数据为 ATRA 诱导的 RIG-G 表达机制提供了新的见解。