下调IRAK1基因调控NF-κB信号通路抑制宫颈癌细胞生长的机制研究

被引：13

作者：

陈建翠 ^{[1
]}

姜琦 ^{[2
]}

机构：

[1] 福建省妇幼保健院宫颈疾病诊治保健中心

[2] 吉林大学中日联谊医院肾内科

来源：

免疫学杂志 | 2019年 / 35卷 / 07期

关键词：

宫颈癌; IRAK1; NF-κB; TNF-α;

D O I：

10.13431/j.cnki.immunol.j.20190091

中图分类号：

R737.33 [子宫肿瘤];

学科分类号：

100214 ;

摘要：

目的探索下调白介素1受体相关激酶1(IRAK1)对宫颈癌细胞恶性生物学特性的影响以及可能作用机制。方法以宫颈癌Caski细胞作为研究对象,在脂质体2000的介导下转染siRNA IRAK1以及阴性对照,正常培养的细胞作为对照,蛋白质印迹法(Western blot)检测转染后Caski细胞中IRAK1蛋白的表达量;噻唑蓝(MTT)检测细胞的增殖活性;脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)检测细胞的凋亡;Transwell以及黏附实验检测细胞的侵袭、黏附能力;荧光定量PCR检测细胞中IRAK1 mRNA以及核因子-κB(NF-κB)mRNA水平;酶联免疫吸附测定法(ELISA)检测肿瘤坏死因子-α(TNF-α)、单核细胞趋化因子蛋白-1(MCP-1)水平。结果转染siRNA IRAK1显著降低细胞中IRAK1的表达量;下调IRAK1能抑制宫颈癌Caski细胞的增殖(P<0.05),诱导其凋亡,降低细胞的侵袭、黏附能力,抑制NF-κB mRNA以及TNF-α、MCP-1水平。结论下调IRAK1可能通过调控NF-κB信号通路抑制宫颈癌Caski细胞的恶性生物学特性,从而抑制宫颈癌细胞的生长。

引用

页码：587 / 592

页数：6

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