首页|亚砷酸钠调控Wnt信号通路抑制口腔鳞状细胞癌增殖及促进凋亡的机制研究

亚砷酸钠调控Wnt信号通路抑制口腔鳞状细胞癌增殖及促进凋亡的机制研究

扫码查看
原文链接
  • NETL
  • NSTL
  • 万方数据
  • 维普
目的 探讨亚砷酸钠调控wnt信号通路对口腔鳞状细胞癌增殖及凋亡的影响.方法 分别采用125、2.5、5、10、20μmol/L 的亚砷酸钠处理人口腔鳞状细胞癌细胞株Tca8113 24、48、72 h,CCK8 实验检测细胞增殖情况.采用0.10 μmol/L 的亚砷酸钠处理Tca8113 细胞48 h 后,流式细胞仪检测细胞凋亡,Western blot 检测Cleaved caspase3、β-catenin、Cyclin D1 蛋白表达.将Tca8113 细胞分为对照组、亚砷酸钠组(10 μmol/L)、激活剂(10 mmol/L 的LiCl)+亚砷酸钠组(10 μmol/L 亚砷酸钠),各组细胞处理48 h 后,CCK8 实验、流式细胞术及Western blot 分别检测3 组细胞增殖、凋亡及Cleaved caspase3、β-catenin、Cyclin D1 蛋白表达.结果 随着作用时间及亚砷酸钠浓度增加,Tca8113 细胞增殖抑制率均显著升高,具有时间和浓度依赖性(P＜0.05或P＜0.01),根据IC50选择10μmol/L的亚砷酸钠作为后续研究.10μmol/L的亚砷酸钠组细胞凋亡率及Cleaved caspase3蛋白表达显著高于0μmol/L组,β-catenin、Cyclin D1蛋白表达显著低于0μmol/L组(P＜.0.01).亚砷酸钠组及激活剂+亚砷酸钠组细胞凋亡率、细胞抑制率及Cleaved caspase3蛋白表达均显著高于对照组,β-catenin、Cyclin D1蛋白表达显著低于对照组(P＜0.01);激活剂+亚砷酸钠组细胞凋亡率、细胞抑制率及Cleaved caspase3蛋白表达均显著低于亚砷酸钠组,β-catenin、Cyclin D1蛋白表达显著高于亚砷酸钠组(P＜.0.01).结论 亚砷酸钠可抑制口腔鳞状细胞癌增殖及促进凋亡,其机制与Wnt信号通路的调控有关.
Mechanism of Sodium arsenite by Wnt signaling pathway inhibits the proliferation of oral squamous cell carcinoma and promote apoptosis
Objective To investigate the effect of sodium arsenite by Wnt signaling pathway on proliferation and apoptosis of oral squamous cell carcinoma.Methods Cell proliferation was detected after 1.25,2.5,5,10,20μmol/L sodium arsenite treatment human oral squamous cell carcinoma cell line Tca8113 for 24,48,72 hours by CCK8 experiment.0 and 14μmol/L sodium arsenite was used to treatment Tca8113 cells with 48h,cell apoptosis were detected by flow cytometry,Cleaved Caspase3,β-catenin,Cyclin D1 protein expression were detected by Western blot.Tca8113 cells were divided into control group,sodium arsenite group,activating agent+sodium arsenite group,all treated for 48hour,cell proliferation,apoptosis and Cleaved Caspase3,β-catenin,Cyclin D1 protein expression were detected by CCK8 assay,flow cytometry and Western blot.Results Tca8113 cell proliferation was inhibited significantly with the increase of treatment time and sodium arsenite concentration,and has a time and concentration dependent manner(P<0.05 or P<0.01).10μmol/L sodium arsenite as a follow-up study according to the IC50.Cell inhibition rate,apoptosis rate and Cleaved Caspase3 protein expression in 10μmol/L group were significantly higher than that of 0 mol/L group,the expression of β-catenin,Cyclin D1 protein was significantly lower than that of 0 mol/L group(P<0.01).Apoptosis rate,cell inhibition rate and Cleaved Caspase 3 protein expression in sodium arsenite group and activating agent+sodium arsenite group were significantly higher than control group,the expression of β-catenin and Cyclin D1 protein were significantly lower than control group(P<0.01).Apoptosis rate,cell inhibition rate and Cleaved Caspase 3 protein expression in activating agent + sodium arsenite group were significantly lower than that of sodium arsenite group,the expression of β-catenin and Cyclin D1 protein were significantly higher than that of sodium arsenite group(P<0.01).Conclusion Sodium arsenite can inhibit the proliferation of oral squamous cell carcinoma and promote apoptosis,and the mechanism was related to regulation of Wnt signaling pathway.

sodium arseniteWnt signaling pathwayoral squamous cell carcinomaproliferationapoptosis

邱峰、王潇悦、赵军方、方政、李新明

展开 >

郑州大学第一附属医院 口腔医学中心,河南 郑州 450052

河南大学 第一临床医学院,河南 开封 475004

亚砷酸钠 Wnt信号通路 口腔鳞状细胞癌 增殖 凋亡

2017

10.3969/j.issn.1005-1678.2017.04.004

中国生化药物杂志
南京生物化学制药研究所,全国生化制药情报中心站,中国生化制药工业协会,中国药品生物制品检定所

中国生化药物杂志

ISSN：1005-1678
年,卷(期)：2017.(4)
  • 2
  • 3