Alternative lengthening of telomeres: remodeling the telomere architecture.
Alternative lengthening of telomeres: remodeling the telomere architecture.
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DOI：
10.3389/fonc.2013.00027
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发表时间：
2013
影响因子：
4.7
通讯作者：
Reddel RR
中科院分区：
文献类型：
--
作者：
Conomos D;Pickett HA;Reddel RR
为了摆脱增殖潜力的正常限制，癌细胞必须采用一种方法来抵消伴随半保守DNA复制的端粒逐渐磨损。虽然大多数人类癌症通过上调端粒酶活性来实现这一点，但其余大多数癌症使用同源重组介导的端粒延长机制，称为端粒替代延长（ALT）。ALT途径的许多分子细节尚不清楚，关于该途径被激活的机制更是知之甚少。在这里，我们回顾了目前的研究结果，端粒结构在ALT细胞，包括DNA序列，shelterin含量，异染色质状态。我们推测端粒结构的重塑可能有助于ALT表型的出现和维持。
To escape from the normal limits on proliferative potential, cancer cells must employ a means to counteract the gradual telomere attrition that accompanies semi-conservative DNA replication. While the majority of human cancers do this by up-regulating telomerase enzyme activity, most of the remainder use a homologous recombination-mediated mechanism of telomere elongation known as alternative lengthening of telomeres (ALT). Many molecular details of the ALT pathway are unknown, and even less is known regarding the mechanisms by which this pathway is activated. Here, we review current findings about telomere structure in ALT cells, including DNA sequence, shelterin content, and heterochromatic state. We speculate that remodeling of the telomere architecture may contribute to the emergence and maintenance of the ALT phenotype.