NF-κB对肺癌细胞生长、细胞周期及肿瘤坏死因子-α分泌的影响  

The effect of NF-κB on the growth,cell cycle and TNF-α secretion of lung cancer cells

作　　者：赵旭[1] 王晓寒[1] 广东 张铭 ZHAO Xu;WANG Xiao-Han;GUANG Dong(Henan Vocational College of Nursing,Anyang 455000,Henan,China)

机构地区：[1]河南护理职业学院,河南安阳455000 [2]大庆市大庆油田总医院 [3]大庆市龙南医院

出　　处：《中国老年学杂志》2018年第17期4223-4226,共4页Chinese Journal of Gerontology

基　　金：国家自然科学基金资助项目(81172717)

摘　　要：目的探讨核因子(NF)-κB对肺癌细胞生长、细胞周期及分泌肿瘤坏死因子(TNF)-α的影响。方法用NF-κB抑制剂SN50处理肺癌细胞,MTT测定细胞增殖,流式细胞术测定细胞周期和细胞凋亡,酶联免疫吸附试验(ELISA)测定培养液上清中TNF-α含量,Western印迹测定细胞中细胞周期蛋白(Cyclin)B1、Cyclin D1、剪切的含半胱氨酸的天冬氨酸蛋白水解酶(酶切Caspase)-3、Bcl-2相关X蛋白(Bax)、NF-κBp65蛋白水平。结果 SN50能够抑制肺癌细胞的增殖,且随着SN50作用浓度和作用时间的增加抑制增殖作用越强。SN50组凋亡率明显高于对照组(P<0.05)。SN50组肺癌细胞G2/M比例明显高于对照组(P<0.05)。SN50组TNF-α水平明显高于对照组(P<0.05),Cyclin B1、Cyclin D1、NF-κBp65蛋白水平明显低于对照组,而酶切Caspase-3、Bax水平明显高于对照组(P<0.05)。结论抑制NF-κB信号通路可以阻碍肺癌细胞增殖,将细胞周期阻滞在G2/M期,诱导细胞凋亡,促进细胞中酶切Caspase-3、Bax表达,下调细胞中Cyclin B1、Cyclin D1蛋白水平。Objective To investigate the effect of NF-κB on the growth,cell cycle and secretion of TNF-α in lung cancer cells.Methods NF-κB inhibitor SN50 was used to treat lung cancer cells,the cell proliferation was tested by MTT,cell cycle and apoptosis were measured by flow cytometry. The content of TNF-α in supernatant of culture liquid was determined by ELISA. Western blot was used to determine the levels of Cyclin B1,Cyclin D1,cleaved Caspase-3,Bax,NF-κBp65 proteins.Results SN50 inhibited the proliferation of lung cancer cells,and with the increasing of SN50 concentration and time.The apoptosis rate of lung cancer cells after SN50 treatment was significantly higher than that of normal lung cancer cells（ P〈0. 05）. The proportion of G2/M in lung cancer cells after SN50 treatment was significantly higher than that of normal lung cancer cells（ P〈0.05）. The level of TNF-α in lung cancer cell culture solution after SN50 treatment was significantly higher than that of normal lung cancer cells（ P〈0.05）. The levels of Cyclin B1,Cyclin D1 and NF-κBp65 in lung cancer cells treated with SN50 were significantly lower than those of normal lung cancer cells. The levels of cleaved Caspase-3 and Bax were significantly higher than those of normal cultured lung cancer cells（ P〈0.05）.Conclusions Inhibition of NF-κB signaling pathway could inhibit the proliferation of lung cancer cells,block cell cycle at G2/M stage,induce apoptosis,promote the expressions of cleaved Caspase-3 and Bax,down-regulate the levels of Cyclin B1 and Cyclin D1 protein.

关 键 词：核因子(NF)-κB 肺癌 细胞周期 肿瘤坏死因子(TNF)-α 

分 类 号：R734.2[医药卫生—肿瘤]