多重p53脉冲破坏细胞周期的机制。

Kazunari Iwamoto, Hiroyuki Hamada, Masahiro Okamoto
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引用次数: 0

摘要

当DNA损伤产生时,肿瘤抑制基因p53被激活,选择细胞周期阻滞、DNA修复、诱导凋亡等细胞命运。最近在MCF7细胞系中观察到p53振荡。然而,p53振荡的生物学意义尚不清楚。在此,我们构建了一个具有p53信号网络的细胞周期调控系统的数学模型来研究p53振荡与细胞周期进程的关系。首先,没有DNA损伤的模拟结果与生物学研究结果一致。接下来,DNA损伤的模拟实现了p53振荡和细胞周期阻滞,并表明多个p53脉冲的产生破坏了细胞周期进程。此外,模拟结果表明,细胞周期中断是由于细胞周期中的M期突变引起的,这是由于周期蛋白A/周期蛋白依赖性激酶2的下降。本研究的结果表明,产生多个p53脉冲对抗DNA损伤可能被用作细胞周期中断的标志。
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Mechanism of cell cycle disruption by multiple p53 pulses.

When the DNA damage is generated, the tumor suppressor gene p53 is activated and selects the cell fate such as the cell cycle arrest, the DNA repair and the induction of apoptosis. Recently, the p53 oscillation was observed in MCF7 cell line. However, the biological meaning of p53 oscillation was still unclear. Here, we constructed a novel mathematical model of cell cycle regulatory system with p53 signaling network to investigate the relationship between the p53 oscillation and the cell cycle progression. First, the simulated result without DNA damage agreed with the biological findings. Next, the simulations with DNA damage realized both the p53 oscillation and the cell cycle arrest, and indicated that the generation of multiple p53 pulses disrupted the cell cycle progression. Moreover, the simulated results showed that the cell cycle disruption was caused by the catastrophe of M phase in the cell cycle, which resulted from the decline in cyclin A/cyclin-dependent kinase 2. The results in this study suggested that the generation of multiple p53 pulses against DNA damage may be used as a marker of cell cycle disruption.

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