Regulation of Myc by miR-34c A mechanism to prevent genomic instability?

被引：49

作者：

Cannell, Ian G. ^{[2
]}

Bushell, Martin ^{[1
]}

机构：

[1] Univ Leicester, MRC Toxicol Unit, Leicester LE1 9HN, Leics, England

[2] MIT, David H Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA

来源：

CELL CYCLE | 2010年 / 9卷 / 14期

关键词：

microRNA; cell cycle; DNA damage; P38; DNA-DAMAGE RESPONSE; C-MYC; TUMOR-SUPPRESSOR; MICRORNA; P53; METHYLATION; TRANSACTIVATION; TRANSFORMATION; REPLICATION; SENESCENCE;

D O I：

10.4161/cc.9.14.12182

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Over the past 8 years several lines of compelling evidence have indicated that microRNAs are critical downstream effectors of classic oncogene/tumour suppressor networks. The archetypal examples of oncogene and tumour suppressor microRNAs are the miR-17-92 (oncomir 1) polycistron and miR-34 respectively. Whilst the involvement of these two opposing families of microRNAs in oncogenesis has been known for some time, the mRNA targets through which they exert their phenotypes are only just beginning to be uncovered. Moreover, several recent reports have demonstrated that the relevant physiological targets of certain individual microRNAs are actually fairly limited, with repression of just one or two major targets sufficient to explain the observed phenotype. In this review we will discuss the emerging role of microRNAs in tumourigenesis with a specific focus on miR-34c-dependent regulation of Myc.

引用

页码：2726 / 2730

页数：5

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