Endogenous retroviral promoter exaptation in human cancer.

Endogenous retroviral promoter exaptation in human cancer.
复制标题

DOI:
10.1186/s13100-016-0080-x
复制
发表时间:
2016
期刊:
影响因子:
4.9
通讯作者:
Mager DL
Mager DL
中科院分区:
生物学3区
文献类型:
--
作者:
Babaian A;Mager DL

文献摘要

参考文献

被引文献

相似文献

癌症由一系列遗传和表观遗传变化引起,这些变化导致癌基因的异常表达或突变激活,以及肿瘤抑制基因的抑制/失活。具有致癌特性的编码基因或长链非编码RNA(lncRNA)的异常表达可由易位、基因扩增、点突变或其他特征较少的机制引起。一种这样的机制是不适当地使用用于驱动致癌基因表达的通常休眠的、组织限制的或隐蔽的增强子或启动子。内源性逆转录病毒(ERV)分布于人类基因组中,提供了大量的自主基因调控模块,其中一些在进化过程中被宿主吸收,在基因和基因网络的正常调控中发挥重要作用。本审查侧重于这种ERV监管能力的“阴暗面”。具体来说,我们讨论了越来越多的正常休眠或表观遗传抑制ERVs的例子,这些ERVs被利用来驱动人类癌症中的癌基因,这是一个我们称之为肿瘤外适应的过程,我们提出了可能导致这种现象的潜在机制。
Cancer arises from a series of genetic and epigenetic changes, which result in abnormal expression or mutational activation of oncogenes, as well as suppression/inactivation of tumor suppressor genes. Aberrant expression of coding genes or long non-coding RNAs (lncRNAs) with oncogenic properties can be caused by translocations, gene amplifications, point mutations or other less characterized mechanisms. One such mechanism is the inappropriate usage of normally dormant, tissue-restricted or cryptic enhancers or promoters that serve to drive oncogenic gene expression. Dispersed across the human genome, endogenous retroviruses (ERVs) provide an enormous reservoir of autonomous gene regulatory modules, some of which have been co-opted by the host during evolution to play important roles in normal regulation of genes and gene networks. This review focuses on the “dark side” of such ERV regulatory capacity. Specifically, we discuss a growing number of examples of normally dormant or epigenetically repressed ERVs that have been harnessed to drive oncogenes in human cancer, a process we term onco-exaptation, and we propose potential mechanisms that may underlie this phenomenon.
DOI: 10.1371/journal.pone.0109478
发表时间: 2014
期刊: PloS one
影响因子: 3.7
作者:
Barchitta M;Quattrocchi A;Maugeri A;Vinciguerra M;Agodi A
通讯作者: Agodi A
DOI: 10.1186/s13100-015-0041-9
发表时间: 2015
期刊: Mobile DNA
影响因子: 4.9
作者:
Bao W;Kojima KK;Kohany O
通讯作者: Kohany O
DOI: 10.1073/pnas.0831042100
发表时间: 2003-04-29
影响因子: 11.1
作者:
Brouha, B;Schustak, J;Kazazian, HH
通讯作者: Kazazian, HH
DOI: 10.1038/onc.2015.308
发表时间: 2016-05-12
期刊: ONCOGENE
影响因子: 8
作者:
Babaian, A.;Romanish, M. T.;Mager, D. L.
通讯作者: Mager, D. L.
DOI: 10.1126/science.aad5497
发表时间: 2016-03-04
期刊: Science (New York, N.Y.)
影响因子: --
作者:
Chuong EB;Elde NC;Feschotte C
通讯作者: Feschotte C