一氧化氮通过诱导 S-G2/M 细胞周期停滞来抑制 Caco-2 细胞的增殖。

International journal of physiology, pathophysiology and pharmacology Pub Date : 2019-10-15 eCollection Date: 2019-01-01
Satoru Sakuma, Yukino Ikeda, Itsumi Inoue, Kanna Yamaguchi, Shohko Honkawa, Tetsuya Kohda, Saaya Minamino, Yohko Fujimoto
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摘要

关于一氧化氮(NO)促进或抑制结直肠癌细胞增殖的能力,目前存在相互矛盾的数据。此外,一氧化氮会以扩散控制速率与内源性超氧化物快速反应,生成过氧化亚硝酸盐(ONOO-),这是一种强氧化剂和硝化剂。本研究旨在评估外源性 NO 和 ONOO- 对结直肠癌细胞系 Caco-2 增殖的影响。NOR5和SIN-1分别用作NO和ONOO-供体。NOR5 和 SIN-1 都能抑制 Caco-2 细胞的增殖,但 NOR5 的作用略强于 SIN-1。结果还表明,NO 在抑制 SIN-1 诱导的 Caco-2 细胞增殖中起着重要作用。末端脱氧核苷酸转移酶 dUTP 缺口标记检测、细胞周期分析和 p21 蛋白表达测定的结果进一步表明,NO 能诱导 Caco-2 细胞 S-G2/M 期停滞,但不能诱导细胞凋亡。结果表明,NO 而不是 ONOO- 有可能通过诱导 S-G2/M 细胞周期停滞来抑制 Caco-2 细胞的增殖。
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Nitric oxide represses the proliferation of Caco-2 cells by inducing S-G2/M cell cycle arrest.

There is conflicting data regarding the ability of nitric oxide (NO) to promote or inhibit colorectal cancer cell proliferation. Furthermore, NO reacts rapidly with endogenous superoxide at a diffusion-controlled rate to give peroxynitrite (ONOO-), a strong oxidant and nitrating agent. The aim of this study was to assess the effects of exogenous NO and ONOO- on the proliferation of the colorectal cancer cell line Caco-2. NOR5 and SIN-1 were used as NO and ONOO- donors, respectively. Both NOR5 and SIN-1 inhibited the proliferation of the Caco-2 cells; however, the effect of NOR5 was slightly stronger than that of SIN-1. The results also indicated that NO plays a major role in the inhibition of SIN-1-induced proliferation of Caco-2 cells. The results of a terminal deoxynucleotidyl transferase dUTP nick end labeling assay, cell cycle analysis, and p21 protein expression measurement further indicated that NO induced S-G2/M phase arrest, but not apoptosis, in the Caco-2 cells. The results suggest that NO, rather than ONOO-, has the potential to repress the proliferation of Caco-2 cells by inducing S-G2/M cell cycle arrest.

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