肿瘤源性细胞系端粒酶活性和端粒长度的克隆异质性。

I Savre-Train, L S Gollahon, S E Holt
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引用次数: 21

摘要

核糖核蛋白,端粒酶,在大多数永生细胞和癌细胞中负责维持端粒长度。端粒酶似乎是人类恶性肿瘤的标志物,至少85%的人类癌症表达其活性。在本研究中,我们检测了一系列肿瘤来源和体外永生化细胞系的端粒酶活性水平、端粒长度、端粒酶的RNA和催化成分的表达水平。我们发现肿瘤细胞克隆的端粒长度和端粒酶活性都有显著的差异。此外,端粒酶成分或端粒酶活性的水平不能预测端粒长度。来自克隆来源细胞的数据表明,这些肿瘤来源细胞系的端粒严重缩短可能通过端粒酶催化亚基表达的增加来激活端粒酶活性。虽然端粒酶低的克隆随着时间的推移会缩短端粒,但它们的亚克隆都具有高水平的端粒酶活性,而端粒不会缩短。此外,对早期克隆端粒酶活性的分析表明,端粒酶具有很大的可变性,这表明单个细胞的活性水平是波动的。我们的数据表明细胞群表现出端粒酶活性的循环表达,这可能部分由端粒缩短调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Clonal heterogeneity in telomerase activity and telomere length in tumor-derived cell lines.

The ribonucleoprotein, telomerase, is responsible for the maintenance of telomere length in most immortal and cancer cells. Telomerase appears to be a marker of human malignancy with at least 85% of human cancers expressing its activity. In the present study, we examined a series of tumor-derived and in vitro immortalized cell lines for telomerase activity levels, telomere lengths, and expression levels of the RNA and catalytic components of telomerase. We found significant variability in both telomere lengths and telomerase activity in clones from tumor cells. In addition, the levels of telomerase components or telomerase activity were not predictive of telomere length. Data from clonally derived cells suggest that critically shortened telomeres in these tumor-derived cell lines may signal activation of telomerase activity through an increase in the expression of the catalytic subunit of telomerase. Although clones with low telomerase shorten their telomeres over time, their subclones all have high levels of telomerase activity with no telomere shortening. In addition, analysis of early clones for telomerase activity indicates substantial variability, which suggests that activity levels fluctuate in individual cells. Our data imply that cell populations exhibit a cyclic expression of telomerase activity, which may be partially regulated by telomere shortening.

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