Nitric oxide represses the proliferation of Caco-2 cells by inducing S-G 2 /M cell cycle arrest.

Autor: Sakuma S; Department of Physiological Chemistry, Osaka University of Pharmaceutical Sciences 4-20-1 Nasahara, Takatsuki 569-1094, Osaka, Japan., Ikeda Y; Department of Physiological Chemistry, Osaka University of Pharmaceutical Sciences 4-20-1 Nasahara, Takatsuki 569-1094, Osaka, Japan., Inoue I; Department of Physiological Chemistry, Osaka University of Pharmaceutical Sciences 4-20-1 Nasahara, Takatsuki 569-1094, Osaka, Japan., Yamaguchi K; Department of Physiological Chemistry, Osaka University of Pharmaceutical Sciences 4-20-1 Nasahara, Takatsuki 569-1094, Osaka, Japan., Honkawa S; Department of Physiological Chemistry, Osaka University of Pharmaceutical Sciences 4-20-1 Nasahara, Takatsuki 569-1094, Osaka, Japan., Kohda T; Department of Physiological Chemistry, Osaka University of Pharmaceutical Sciences 4-20-1 Nasahara, Takatsuki 569-1094, Osaka, Japan., Minamino S; Department of Physiological Chemistry, Osaka University of Pharmaceutical Sciences 4-20-1 Nasahara, Takatsuki 569-1094, Osaka, Japan., Fujimoto Y; Department of Physiological Chemistry, Osaka University of Pharmaceutical Sciences 4-20-1 Nasahara, Takatsuki 569-1094, Osaka, Japan.
Jazyk: angličtina
Zdroj: International journal of physiology, pathophysiology and pharmacology [Int J Physiol Pathophysiol Pharmacol] 2019 Oct 15; Vol. 11 (5), pp. 205-211. Date of Electronic Publication: 2019 Oct 15 (Print Publication: 2019).
Abstrakt: 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-G 2 /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-G 2 /M cell cycle arrest.
Competing Interests: None.
(IJPPP Copyright © 2019.)
Databáze: MEDLINE
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