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首页> 外文期刊>Life sciences >Telomerase activity is not related to apoptosis in leukemic cell lines.
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Telomerase activity is not related to apoptosis in leukemic cell lines.

机译：端粒酶活性与白血病细胞系中的细胞凋亡无关。

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Any deregulation of apoptosis or an escape from cellular senescence will drive the cells to neoplasia. It remains unclear whether there is a direct linkage between apoptosis and telomerase activity particularly in transformed cell lines. In the present study, we investigated the telomerase activities in three leukemic cell lines (HL-60, U937 and K562) after treating these cells with various doses of antitumor drugs, puromycin or actinomycin D (ActD). Our results showed that HL-60 cells underwent apoptosis rapidly when treated with either 20 microg/ml of puromycin or 5 microg/ml of Act D with more than 60% of the cells becoming apoptotic at 6 hrs and almost 100% at 12 hrs. But telomerase activity analyzed by TRAP assay in these apoptotic cells remained unchanged as compared with the untreated control cells suggesting that whether the cells were apoptotic or not, it had no effect on telomerase activity. However, if lower dosages of the drugs were used, that is, 0.5-1.5 microg/ml of puromycin or 0.01-0.5 microg/ml of Act D, a decrease in telomerase activity was observed at 24-48 hrs, and was completely undetectable at 72 hrs. This decrease in telomerase activity was dose- and time-dependent. The suppression of telomerase activity by low doses of these two drugs is probably due to the inhibitory effect of the drugs on protein translation or RNA transcription rather than direct inhibition of the telomerase activity. Flow cytometry analysis of the cell cycle of the drug-treated cells showed that these drugs unselectively induced apoptosis at all phases of the cell cycle and was unrelated to the changes in telomerase activity. Similar results were observed in U937 and K562 cells except that K562 cells underwent apoptosis more slowly than the former two cell lines.
机译：凋亡的任何失调或细胞衰老的逃逸都将驱动细胞向肿瘤形成。尚不清楚凋亡与端粒酶活性之间是否存在直接联系，尤其是在转化的细胞系中。在本研究中，我们用不同剂量的抗肿瘤药，嘌呤霉素或放线菌素D（ActD）处理了三种白血病细胞系（HL-60，U937和K562）后，研究了它们的端粒酶活性。我们的结果表明，当用20微克/毫升的嘌呤霉素或5微克/毫升的Act D处理时，HL-60细胞迅速凋亡，其中60％以上的细胞在6小时时凋亡，而在12小时时几乎100％凋亡。但是，与未处理的对照细胞相比，通过TRAP测定分析的这些凋亡细胞中的端粒酶活性保持不变，表明该细胞是否具有凋亡性，对端粒酶活性没有影响。但是，如果使用较低剂量的药物，即嘌呤霉素为0.5-1.5微克/毫升或Act D为0.01-0.5微克/毫升，则在24-48小时观察到端粒酶活性下降，这是完全无法检测到的在72小时端粒酶活性的这种降低是剂量和时间依赖性的。低剂量的这两种药物对端粒酶活性的抑制可能是由于这些药物对蛋白质翻译或RNA转录的抑制作用，而不是端粒酶活性的直接抑制。对药物处理过的细胞的细胞周期进行流式细胞术分析表明，这些药物在细胞周期的所有阶段均非选择性诱导细胞凋亡，并且与端粒酶活性的变化无关。在U937和K562细胞中观察到了相似的结果，除了K562细胞凋亡的速度比前两个细胞系慢。

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