UV-induced DNA repair in leukemic cell differentiation.

T Nakamaki, T Ajiri, A Sakashita, S Tomoyasu, N Tsuruoka
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Abstract

Ultraviolet light (UV)-induced DNA repair during myeloid leukemic cell differentiation was examined. Human myeloid leukemic cells could be induced to differentiate in vitro into mature cells by various chemical inducers that lost their proliferating potencies. In spite of decrease of proliferation capacity, almost all these terminally differentiated myeloid leukemic cells invariably showed UV-induced unscheduled DNA synthesis (UDS) at low energy of UV irradiation (3-5J/m2). This indicated that the terminally differentiated myeloid leukemic cells are functionally quite different from mature granulocytes in chronic myeloid leukemia (CML) or in normal peripheral blood. In HL-60 cells, UV-survival was enhanced in the process of differentiation induced by 1.25% DMSO or 0.6 mM sodium n-butyrate. The degree of enhancement of UV-survival was correlated with the increased amount of UDS. The process of myeloid leukemic cell differentiation which is completed without loss of capacity performing repair DNA synthesis was one of the characteristics of the terminally differentiated myeloid leukemic cells induced by chemical inducers in vitro and this function may support the hypothesis that DNA breaking and rejoining are involved in a mechanism of cytodifferentiation.

紫外线诱导的白血病细胞分化中的DNA修复。
研究了紫外光(UV)诱导的髓系白血病细胞分化过程中的DNA修复。人类髓系白血病细胞可以通过各种化学诱导剂在体外诱导分化为成熟细胞,但失去了增殖能力。尽管增殖能力下降,但在低能量(3-5J/m2)的紫外线照射下,几乎所有这些终末分化的髓系白血病细胞都表现出紫外线诱导的非预定DNA合成(UDS)。这表明终末分化的髓系白血病细胞在功能上与慢性髓系白血病(CML)或正常外周血中的成熟粒细胞有很大不同。在HL-60细胞中,1.25%的DMSO和0.6 mM的正丁酸钠诱导的分化过程中,紫外线存活率提高。UV-survival的增强程度与UDS的增加有关。髓系白血病细胞在体外化学诱导剂诱导的终分化髓系白血病细胞的特征之一是在不丧失修复DNA合成能力的情况下完成分化,这一功能可能支持了DNA断裂和重新连接参与细胞分化机制的假设。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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