E2F1 up-regulates the expression of the tumour suppressor axin2 both by activation of transcription and by mRNA stabilisation

被引：16

作者：

Hughes, TA ^{[1
]}

Brady, HJM ^{[1
]}

机构：

[1] UCL, Inst Child Hlth, Mol Haematol & Canc Biol Unit, London, England

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2005年 / 329卷 / 04期

基金：

英国医学研究理事会;

关键词：

axin2; E2F1; Wnt; mRNA stability; HuR; post-transcriptional regulation;

D O I：

10.1016/j.bbrc.2005.02.102

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Axin2 is a negative regulator of Wnt/beta-catenin signalling with roles in early development and tumour suppression. Axin2 is induced by E2F1 and therefore acts as a point of cross-talk between the pRb/E2F and Wnt/beta-catenin pathways: two of the most frequently deregulated pathways in human cancers. In this study, we show that E2F1 up-regulates axin2 by two independent mechanisms. The human axin2 gene allows transcription of messages with three different 5' untranslated regions and in the first mechanism E2F1 directly activates the transcription of only one of these species by acting at canonical E2F binding sites. Second, E2F1 induces stabilisation of axin2 mRNAs. We discuss this regulation with respect to other known E2F targets. (c) 2005 Elsevier Inc. All rights reserved.

引用

页码：1267 / 1274

页数：8

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