{"title":"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。","authors":"Satoru Sakuma, Yukino Ikeda, Itsumi Inoue, Kanna Yamaguchi, Shohko Honkawa, Tetsuya Kohda, Saaya Minamino, Yohko Fujimoto","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>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<sup>-</sup>), a strong oxidant and nitrating agent. The aim of this study was to assess the effects of exogenous NO and ONOO<sup>-</sup> on the proliferation of the colorectal cancer cell line Caco-2. NOR5 and SIN-1 were used as NO and ONOO<sup>-</sup> 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<sub>2</sub>/M phase arrest, but not apoptosis, in the Caco-2 cells. The results suggest that NO, rather than ONOO<sup>-</sup>, has the potential to repress the proliferation of Caco-2 cells by inducing S-G<sub>2</sub>/M cell cycle arrest.</p>","PeriodicalId":94056,"journal":{"name":"International journal of physiology, pathophysiology and pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2019-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6872484/pdf/","citationCount":"0","resultStr":"{\"title\":\"Nitric oxide represses the proliferation of Caco-2 cells by inducing S-G<sub>2</sub>/M cell cycle arrest.\",\"authors\":\"Satoru Sakuma, Yukino Ikeda, Itsumi Inoue, Kanna Yamaguchi, Shohko Honkawa, Tetsuya Kohda, Saaya Minamino, Yohko Fujimoto\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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<sup>-</sup>), a strong oxidant and nitrating agent. The aim of this study was to assess the effects of exogenous NO and ONOO<sup>-</sup> on the proliferation of the colorectal cancer cell line Caco-2. NOR5 and SIN-1 were used as NO and ONOO<sup>-</sup> 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<sub>2</sub>/M phase arrest, but not apoptosis, in the Caco-2 cells. The results suggest that NO, rather than ONOO<sup>-</sup>, has the potential to repress the proliferation of Caco-2 cells by inducing S-G<sub>2</sub>/M cell cycle arrest.</p>\",\"PeriodicalId\":94056,\"journal\":{\"name\":\"International journal of physiology, pathophysiology and pharmacology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-10-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6872484/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International journal of physiology, pathophysiology and pharmacology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2019/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of physiology, pathophysiology and pharmacology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2019/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
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.