Telomeric recombination induced by dysfunctional telomeres.
Telomeric recombination induced by dysfunctional telomeres.
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DOI：
10.1091/mbc.e10-02-0173
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发表时间：
2011-01-15
影响因子：
3.3
通讯作者：
Autexier C
中科院分区：
文献类型：
--
作者：
Brault ME;Autexier C
在人类癌细胞中，在端粒酶阴性的端粒选择性延长中以及在端粒酶抑制或基因缺失后，已经观察到端粒重组。这项研究表明，在端粒酶阳性细胞中，端粒重组机制也可以被功能失调的端粒激活，而不需要端粒酶抑制。 端粒的维持对于细胞的永生是必不可少的，大多数癌细胞通过端粒酶来维持它们的端粒。端粒和端粒酶代表有前途的抗癌靶点。然而，15%的癌细胞通过替代的基于重组的机制来维持其端粒，并且先前的分析表明，基于重组的端粒维持可以在端粒酶抑制后被激活。我们确定端粒重组是否也可以促进端粒功能障碍。我们首次报道了端粒功能失调的人端粒酶阳性癌细胞可以诱导端粒重组。
Telomeric recombination has been observed in telomerase-negative alternative lengthening of telomeres in human cancer cells and following telomerase inhibition or gene deletion. This study shows that telomeric recombination mechanisms can also be activated by dysfunctional telomeres without telomerase inhibition in telomerase-positive cells. Telomere maintenance is essential for cellular immortality, and most cancer cells maintain their telomeres through the enzyme telomerase. Telomeres and telomerase represent promising anticancer targets. However, 15% of cancer cells maintain their telomeres through alternative recombination-based mechanisms, and previous analyses showed that recombination-based telomere maintenance can be activated after telomerase inhibition. We determined whether telomeric recombination can also be promoted by telomere dysfunction. We report for the first time that telomeric recombination can be induced in human telomerase-positive cancer cells with dysfunctional telomeres.