尼克酰胺对膀胱癌细胞的作用及其机制  

Effect of nicotinamide on bladder cancer cells and its mechanism

作　　者：胡清烜 陈亮[1] 王刚[1] 曹锐 钱开宇 肖宇[1,3] 王行环 

机构地区：[1]武汉大学附属中南医院泌尿外科,湖北武汉430071 [2]武汉市第五医院泌尿外科,湖北武汉430050 [3]武汉大学中南医院精准医学实验室,湖北武汉430071

出　　处：《现代泌尿外科杂志》2017年第12期942-946,共5页Journal of Modern Urology

摘　　要：目的探究尼克酰胺对膀胱癌细胞的作用及其机制。方法采用浓度梯度的尼克酰胺对膀胱癌细胞系UM-UC-3及T24行加药处理,采用MTT实验、流式细胞检测、Transwell实验检测其表型并与对照组对比,Western blot检测特定相关蛋白加药后改变以探究其作用机制。结果加入尼克酰胺后两种膀胱癌细胞系均出现增殖能力下降、细胞周期G0/G1期阻滞、迁移能力下降、且浓度越高越明显。并且周期相关蛋白Cyclin D1,CDK2,CDK4,CDK6和EMT(上皮-间质转化)相关蛋白E-Cadherin和Vimentin均出现相应改变。结论尼克酰胺可以抑制膀胱癌细胞系的增殖和迁移,并且诱导其G0/G1期周期阻滞,对迁移的抑制是通过对EMT的抑制引起的。Objective To explore the effect of nicotinamide （NAM） on bladder cancer cell lines and the mechanism behind it. Methods The bladder cancer cell lines UM-UC-3 and T24 were treated with different concentration of NAM. The phenotypes were detected with MTT assay, flow cytometry and Transwell migration assay. The results were compared with those of the negative control group. Western blot was used to determine the protein alteration. Results The proliferation and migration were both inhibited in both UM-UC-3 and T24 after treatment of NAM,in a dose-dependent manner. The proteins including Cyclin D1 ,CDK2,CDK4,CDK6 and Vimentin were downregulated while E-Cadherin was upregulated in NAM- treated group. Oonclusion NAM inhibited the proliferation and migration of UM-UC-3 and T24,and induced cell cycle arrest at G0/G1 phase. The inhibition of migration was supposed to be done via the inhibition of epithelial-mesenchymal transition （EMT）.

关 键 词：膀胱癌 尼克酰胺 烟酰胺 增殖 细胞周期 迁移 上皮-间质转化 

分 类 号：R737.14[医药卫生—肿瘤]