MicroRNAs, wild-type and mutant p53 More questions than answers

被引：45

作者：

Jones, Matthew Fletcher ^{[1
]}

Lal, Ashish ^{[1
]}

机构：

[1] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA

来源：

RNA BIOLOGY | 2012年 / 9卷 / 06期

基金：

美国国家卫生研究院;

关键词：

miRNA; p53; mutant p53; wild-type p53; cancer; miRNA dysregulation; EPITHELIAL-MESENCHYMAL TRANSITION; TUMOR-SUPPRESSOR P53; DOWN-REGULATION; MIR-200; FAMILY; E-CADHERIN; MIR-34A CONTRIBUTES; NEGATIVE REGULATION; TARGET RECOGNITION; CELL-PROLIFERATION; MIR-17-92; CLUSTER;

D O I：

10.4161/rna.20146

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：

The tumor suppressor p53 is a sequence-specific transcription factor that activates the expression of genes involved in apoptosis, cell cycle arrest and senescence. p53 can also inhibit gene expression and this effect is partly mediated by inducing several microRNAs (miRNAs). MiRNAs have emerged as a new class of regulators of the expression and function of eukaryotic genomes. Tumor suppressive or oncogenic functions have been attributed to some miRNAs. Recent studies have shown that p53 can alter the transcription of several miRNAs, and in some cases, it can also influence miRNA maturation. Conversely, miRNAs can also modulate the abundance and activity of p53 by direct or indirect mechanisms. Moreover, mutant p53 can actively repress the expression of some miRNAs that are activated by wild-type p53. In this review, we discuss recent evidences of this crosstalk between miRNAs and the p53 network and also highlight its implications in cancer.

引用

页码：781 / 791

页数：11

共 156 条

[81] miR-24 Inhibits Cell Proliferation by Targeting E2F2, MYC, and Other Cell-Cycle Genes via Binding to "Seedless" 3′UTR MicroRNA Recognition Elements [J].