阳离子转运调控样蛋白1对肝癌细胞铁死亡的调控及其机制研究  

Regulation of cation transport regulator-like protein on iron death in liver cancer cells and its mechanism

作　　者：庄菊花 王国玉 何赛飞 叶颖[2] 张苗[2] 宋雅楠[2] 夏伟[1] Zhuang Juhua;Wang Guoyu;He Saifei;Ye Ying;Zhang Miao;Song Yanan;Xia Wei(Department of Nuclear Medicine,the Seventh People′s Hospital,Shanghai University of Traditional Chinese Medicine,Shanghai 200137,China;不详)

机构地区：[1]上海中医药大学附属第七人民医院核医学科,200137 [2]上海中医药大学附属第七人民医院中心实验室,200137

出　　处：《山西医药杂志》2021年第18期2626-2628,共3页Shanxi Medical Journal

基　　金：上海市卫生健康委青年项目(20174Y0044);上海市浦东新区科技发展基金(PKJ2017-Y14);上海市浦东新区卫生健康委重点学科建设项目(PWZxk2017-06);上海中医药大学附属第七人民医院人才培养计划(QMX2017-01)。

摘　　要：目的探讨阳离子转运调控样蛋白(CHAC)1对肝癌细胞铁死亡的调控及其作用机制。方法以人肝癌HepG2细胞为研究对象,通过外源性转染CHAC1的过量表达载体,调控CHAC1的表达,同时给予铁死亡诱导剂Erastin,通过噻唑蓝(MTT)比色法检测细胞铁死亡情况。结果上调CHAC1的表达,可使肝癌细胞生长能力下降,与对照组细胞相比,差异有统计学意义(P<0.05)。蛋白质印迹法分析显示,siRNA抑制CHAC1降低细胞内核因子(NF)-κB p65的磷酸化,而外源性的过表达CHAC1后能增加细胞内NF-κB p65的磷酸化。结论上调CHAC1的表达可显著增加肝癌细胞的铁死亡,其分子机制与增加肝癌细胞的NF-κB p65的磷酸化相关。Objective To investigate the regulation of cation transport regulator-like protein(CHAC)1 on iron death in liver cancer cells and its mechanism of action.Methods Human liver cancer HepG2 cells were used as the research objects,and the expression of CHAC1 was regulated by exogenous transfection of CHAC1 overexpression vector.At the same time,the iron death inducer Eratin was given to detect the iron death of the cells by MMT method.Results Up-regulating the expression of CHAC1 can decrease the growth ability of hepatoma cells,which is statistically significant compared with the control cells(P<0.05).Western blotting analysis showed that siRNA knockdown CHAC1 reduced intracellular NF-κB p65 phosphorylation,and exogenous overexpression of CHAC1 increased intracellular NF-κB p65 phosphorylation.Conclusion Up-regulating the expression of CHAC1 can significantly increase iron death in HCC cells,and its molecular mechanism is related to increasing the phosphorylation of NF-κB p65 in HCC cells.

关 键 词：铁死亡 肝肿瘤 阳离子转运蛋白质内 

分 类 号：R735.7[医药卫生—肿瘤]