摘要
目的:探讨二甲双胍对人鼻咽癌C666-1细胞增殖和调亡的作用,并初步研究其作用机制。方法:体外培养人鼻咽癌C666-1细胞,以剂量5,10,20mM的二甲双胍干预细胞24h或48h。采用MTT法检测细胞增殖,流式细胞仪检测细胞凋亡,Real-time PCR检测Bax、Bcl-2和Caspase-3表达。结果:二甲双胍抑制C666-1细胞增殖,随剂量增加和干预时间延长,细胞增殖的抑制作用增强(P<0.05)。二甲双胍诱导C666-1细胞早期凋亡,有剂量效应关系,20mM的二甲双胍干预细胞24h,细胞早期凋亡率(12.40±1.01)%,高于对照组的(7.20±0.53)%,差异有统计学意义(P<0.05)。二甲双胍诱导C666-1细胞Caspase-3表达上调,降低Bcl-2/Bax比值。结论:二甲双胍抑制人鼻咽癌C666-1细胞增殖,诱导其凋亡,其机制可能与调节凋亡相关基因Bax、Bcl-2和Caspase-3的表达有关。
Objective. To explore the effects of metformin on proliferation and apoptosis in human nasopharyngeal carcinoma cell line C666-1. Methods. Human nasopharyngeal carcinoma cell line C666-1 was cultured in vitro and with dose of 5, 10, 20 mM metformin interventing cells for 24 h or 48 h. Then cell proliferation was detected by MTT assay, while the cell apoptosis was measured by flow cytometry, Real-time PCR was applied to detect the expression of Bax,Bcl-2 and Caspase-3 mRNA. Metformin inhibited the proliferation of C666-1 cells, along with the increase of the dose and intervention time prolonged, enhanced the inhibition of cell proliferation（P〈0.05）. Metformin induced early apoptosis of C666-1 cells, with a dose effect relationship, cells intervened by 20 mM metformin for 24 h, early apoptosis rate was （12.40± 1.01）%, which was significantly higher than that of the control group （7.20±0.53）%, the difference was statistically significant （P〈0.05）. Meanwhile, the metformin up-regulated the Caspase-3expression of C666-1 cells, decreased the ratio of Bcl-2/Bax. Conclusion. Metformin could inhibit the growth and induce apoptosis of C666-1 cells, which mechanism may be related to its regulation of expression of apoptosis-related genes Box, Bcl-2 and Caspase-3.
出处
《华夏医学》
CAS
2014年第1期5-8,共4页
Acta Medicinae Sinica
基金
国家自然科学基金资助项目(81260343)
广西教育厅高校科研立项项目(2013LX082)
关键词
二甲双胍
鼻咽癌
凋亡
增殖
metformin
nasopharyngeal carcinoma
apoptosis
proliferation
