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抗白血病药物对CCRF-CEM白血病细胞核基质结合DNA复制的影响。

Effects of antileukemia agents on nuclear matrix-bound DNA replication in CCRF-CEM leukemia cells.

作者信息

Fernandes D J, Smith-Nanni C, Paff M T, Neff T A

机构信息

Department of Biochemistry, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina 27103.

出版信息

Cancer Res. 1988 Apr 1;48(7):1850-5.

PMID:3349463
Abstract

The effects of various antileukemic agents on DNA replication associated with the nuclear matrix were investigated in CCRF-CEM leukemia cells. Residual nuclear matrices were prepared by sequential treatment of nuclei with 1.5 M NaCl, DNase I, and Triton X-100 and contained 1-5, 10, and 37% of the total nuclear DNA, protein, and phospholipid, respectively. In control cells pulse-labeled for 45 s with [3H]thymidine, the specific activity of nascent DNA was four-fold greater in the nuclear matrix fraction relative to the specific activity of the high salt-soluble (nonmatrix) DNA fraction. Pulse-labeling and reconstitution experiments indicated that this enrichment of newly replicated DNA on the nuclear matrix did not result from aggregation of nascent DNA with the matrix. A 2-h incubation of tumor cells with either 0.1 microM teniposide (VM-26), 0.2 microM VM-26, or 0.5 microM amsacrine (m-AMSA) reduced the relative specific activity of nascent DNA on the nuclear matrix by 59, 61, and 54%, respectively, compared to control cells. In contrast hydroxyurea and cytosine arabinoside, at concentrations that markedly inhibited total nuclear DNA synthesis, did not decrease the relative specific activity of newly replicated DNA on the matrix. The results provide evidence that the antiproliferative effects of the DNA topoisomerase II inhibitors, VM-26 and m-AMSA, are localized on the nuclear matrix of CCRF-CEM leukemia cells.

摘要

在CCRF-CEM白血病细胞中研究了各种抗白血病药物对与核基质相关的DNA复制的影响。通过用1.5M NaCl、DNA酶I和 Triton X-100依次处理细胞核来制备残留核基质,其分别含有总核DNA、蛋白质和磷脂的1-5%、10%和37%。在用[3H]胸苷脉冲标记45秒的对照细胞中,相对于高盐可溶性(非基质)DNA组分的比活性,新生DNA在核基质组分中的比活性高四倍。脉冲标记和重组实验表明,新生DNA在核基质上的这种富集不是新生DNA与基质聚集的结果。与对照细胞相比,用0.1微摩尔替尼泊苷(VM-26)、0.2微摩尔VM-26或0.5微摩尔安吖啶(m-AMSA)孵育肿瘤细胞2小时,分别使核基质上新生DNA的相对比活性降低了59%、61%和54%。相比之下,羟基脲和阿糖胞苷在明显抑制总核DNA合成的浓度下,并没有降低基质上新复制DNA的相对比活性。结果提供了证据表明DNA拓扑异构酶II抑制剂VM-26和m-AMSA的抗增殖作用定位于CCRF-CEM白血病细胞的核基质上。

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