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首页> 外文期刊>Journal of Cellular Physiology >Reduction of telomerase activity in human liver cancer cells by a histone deacetylase inhibitor.
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Reduction of telomerase activity in human liver cancer cells by a histone deacetylase inhibitor.

机译：减少人类肝脏的端粒酶活性表达情况癌症细胞组蛋白脱乙酰酶抑制剂。

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摘要

The presence of telomerase has been demonstrated recently in many different malignancies. Several reports documented that in human hepatocellular carcinoma, the level of telomerase activity parallels its differentiation stage. In the present study, the effect of the differentiation-inducing agent sodium butyrate on telomerase activity in four human liver cancer cell lines was investigated using the telomeric repeat amplification protocol. We assayed telomerase activity before and after butyrate treatment and in cell cycle synchronized non-dividing quiescent cells. In addition, telomerase reverse transcriptase levels were measured at the mRNA level. All four cell lines possessed high but not identical levels of telomerase activity. Telomerase activity was significantly reduced by treatment with sodium butyrate as well as trichostatin A in a dose- and time-dependent fashion, paralleling the reduction of cell proliferation. Although methotrexate, hydroxyurea, and colchicine synchronized the cell cycle at G1, S, and G2/M, respectively, and thereby also caused proliferating cells to cease dividing and become quiescent, in this case telomerase activity remained essentially unaltered compared to the control cultures. Moreover, levels of mRNA encoding telomerase reverse transcriptase were not always significantly altered by either sodium butyrate treatment or cell cycle synchronization. These results suggest that sodium butyrate, as a histone deacetylase inhibitor, effectively reduces telomerase activity without affecting transcription levels of the reverse transcriptase component. Copyright 2001 Wiley-Liss, Inc.
机译：端粒酶的存在已被证实最近在许多不同的恶性肿瘤。报告记录,在人类肝细胞癌,端粒酶活性水平相似的分化阶段。本研究的影响differentiation-inducing代理丁酸钠端粒酶活性在四个人类肝癌细胞系使用特性的研究重复放大协议。丁酸前后端粒酶活性表达情况治疗和细胞周期同步非区分静止细胞。端粒酶逆转录酶水平在mRNA水平来衡量。拥有高但不相同的水平端粒酶活性。大大减少了钠治疗丁酸以及trichostatin剂量-一分之一时间的方式,将减少细胞增殖。羟基脲和秋水仙碱细胞同步年代周期在G1, G2 / M,分别从而也导致增殖细胞停止分裂,成为静止的,在这种情况下端粒酶活性基本保持相比没有改变控制文化。此外,信使rna编码端粒酶水平逆转录酶并不总是通过丁酸钠而发生明显改变治疗或细胞周期同步。结果表明,丁酸钠作为组蛋白脱乙酰酶抑制剂,有效降低了端粒酶活性没有影响逆转录酶的转录水平组件。

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