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在缺乏p21的细胞中,抗癌药物诱导的S期与有丝分裂的解偶联。

Uncoupling of S phase and mitosis induced by anticancer agents in cells lacking p21.

作者信息

Waldman T, Lengauer C, Kinzler K W, Vogelstein B

机构信息

The Howard Hughes Medical Institute, Johns Hopkins Oncology Center, and Program in Human Genetics, Baltimore, Maryland 21231, USA.

出版信息

Nature. 1996 Jun 20;381(6584):713-6. doi: 10.1038/381713a0.

Abstract

Precise coordination of the S and M phases of the eukaryotic cell cycle is critical not only for normal cell division, but also for effective growth arrest under conditions of stress. When damaged, a cell must communicate signals to both the mitotic and DNA synthesis machineries so that a mitotic block is not followed by an extra S phase, or vice versa. The biochemical mechanisms regulating this coordination, termed checkpoints, have been identified in lower eukaryotes, but are largely unknown in mammalian cells. Here we show that p21 WAF1/CIP1, the prototype inhibitor of cyclin-dependent kinases (CDKs), is required for this coordination in human cells. In the absence of p21, DNA-damaged cells arrest in a G2-like state, but then undergo additional S phases without intervening normal mitoses. They thereby acquire grossly deformed, polyploid nuclei and subsequently die through apoptosis. Perhaps not by coincidence, the DNA-damaging agents that can cause S/M uncoupling are used in the clinic to kill cancer cells preferentially.

摘要

真核细胞周期中S期和M期的精确协调不仅对正常细胞分裂至关重要,而且在应激条件下对有效的生长停滞也很关键。细胞受损时,必须向有丝分裂和DNA合成机制传递信号,以便有丝分裂阻滞之后不会紧接着出现额外的S期,反之亦然。调节这种协调的生化机制,即检查点,已在低等真核生物中得到鉴定,但在哺乳动物细胞中大多未知。我们在此表明,细胞周期蛋白依赖性激酶(CDK)的原型抑制剂p21 WAF1/CIP1在人类细胞的这种协调中是必需的。在缺乏p21的情况下,DNA受损细胞停滞在类似G2的状态,但随后会经历额外的S期,而没有正常的有丝分裂过程。它们由此获得严重变形的多倍体细胞核,随后通过凋亡死亡。也许并非巧合的是,临床上用于优先杀死癌细胞的DNA损伤剂会导致S/M解偶联。

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