去氧精胍菌素对小鼠白血病细胞系L1210的细胞生长抑制作用。
Cytostatic effect of deoxyspergualin on a murine leukemia cell line L1210.
作者信息
Hiratsuka M, Kuramochi H, Takahashi K, Takeuchi T, Oshimura M
机构信息
Research Laboratories, Pharmaceuticals Group, Nippon Kayaku Co., Ltd., Tokyo.
出版信息
Jpn J Cancer Res. 1991 Oct;82(10):1065-8. doi: 10.1111/j.1349-7006.1991.tb01758.x.
The mode of antiproliferative action of deoxyspergualin (NKT-01) was examined. The growth-inhibitory effect on a murine leukemia cell line L1210 following treatment with NKT-01 was time-dependent, and there was little or no effect on the syntheses of DNA and RNA. Thus, the inhibitory activity of NKT-01 was not attributable to the inhibition of DNA and RNA syntheses. The influence of NKT-01 on cell cycle progression was studied by flow cytometric analysis. Bromodeoxyuridine/DNA distribution patterns in cells that were treated for 72 h, showed that the growth inhibition is due to the delay of cell cycle progression but not to cytotoxicity. This finding was also supported by evidence that the treated cells were re-proliferative in fresh medium. In addition, a majority of drug-treated cells was prevented from traversing from the G0/G1 phase to the S phase by 144 h or longer exposure to NKT-01. The results suggest that NKT-01 is cytostatic, preventing G0/G1-S progression.
研究了脱氧精胍菌素（NKT-01）的抗增殖作用模式。用NKT-01处理后，对小鼠白血病细胞系L1210的生长抑制作用呈时间依赖性，对DNA和RNA的合成几乎没有影响。因此，NKT-01的抑制活性并非归因于对DNA和RNA合成的抑制。通过流式细胞术分析研究了NKT-01对细胞周期进程的影响。经72小时处理的细胞中溴脱氧尿苷/DNA分布模式表明，生长抑制是由于细胞周期进程延迟而非细胞毒性所致。处理后的细胞在新鲜培养基中能够重新增殖这一证据也支持了这一发现。此外，通过144小时或更长时间暴露于NKT-01，大多数药物处理的细胞被阻止从G0/G1期进入S期。结果表明，NKT-01具有细胞生长抑制作用，可阻止G0/G1-S期进程。
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