L1 retrotransposons, cancer stem cells and oncogenesis

被引：71

作者：

Carreira, Patricia E. ^{[1
]}

Richardson, Sandra R. ^{[1
]}

Faulkner, Geoffrey J. ^{[1
,2
]}

机构：

[1] Mater Med Res Inst, Canc Biol Program, South Brisbane, Qld 4101, Australia

[2] Univ Queensland, Sch Biomed Sci, Brisbane, Qld, Australia

来源：

FEBS JOURNAL | 2014年 / 281卷 / 01期

基金：

澳大利亚国家健康与医学研究理事会;

关键词：

Alu; cancer genomics; EMT; L1; LINE-1; oncogenesis; plasticity; retrotransposon; SVA; tumorigenesis; DETECTABLE CLONAL MOSAICISM; HUMAN LINE-1 PROTEIN; TRANSPOSABLE ELEMENTS; SOMATIC RETROTRANSPOSITION; REVERSE TRANSCRIPTION; SMALL RNAS; IDENTIFICATION; HYPOMETHYLATION; REVEALS; METHYLATION;

D O I：

10.1111/febs.12601

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：

Retrotransposons have played a central role in human genome evolution. The accumulation of heritable L1, Alu and SVA retrotransposon insertions continues to generate structural variation within and between populations, and can result in spontaneous genetic disease. Recent works have reported somatic L1 retrotransposition in tumours, which in some cases may contribute to oncogenesis. Intriguingly, L1 mobilization appears to occur almost exclusively in cancers of epithelial cell origin. In this review, we discuss how L1 retrotransposition could potentially trigger neoplastic transformation, based on the established correlation between L1 activity and cellular plasticity, and the proven capacity of L1-mediated insertional mutagenesis to decisively alter gene expression and functional output.

引用

页码：63 / 73

页数：11

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