IscU2对非小细胞肺癌增殖、迁移、侵袭能力的影响及其作用机制的研究  

The Effects and Mechanism of IscU2 on Cell Proliferation,Migration and Invasion Ability in Non-small Cell Lung Cancer Cells

作　　者：韩琴霞 孙倩倩[1,2] 林子帆[1] 周怀彬 吕建新[1] HAN Qinxia;SUN Qianqian;LIN Zifan;ZHOU Huaibin;Lu Jianxin(School of Laboratory Medicine and Life Sciences,Wenzhou Medical University,Wenzhou 325035,China;The Affiliated Hospital of Qingdao University,Qingdao 266000,China)

机构地区：[1]温州医科大学检验医学院,生命科学学院,温州325035 [2]青岛大学附属医院,青岛266000

出　　处：《中国细胞生物学学报》2020年第1期16-25,共10页Chinese Journal of Cell Biology

基　　金：国家自然科学基金(批准号:31670784)资助的课题。

摘　　要：该文通过shRNA干扰技术敲低IscU2干扰细胞IscU2的表达,研究了干扰IscU2对非小细胞肺癌(NSCLC)细胞NCI-H520增殖、迁移及侵袭能力的影响。构建了稳定低表达IscU2的非小细胞肺癌细胞系NCI-H520;采用CCK-8和平板克隆实验检测细胞的增殖能力;流式细胞仪检测细胞周期、凋亡、ROS、线粒体膜电位变化情况;Transwell实验检测细胞迁移及侵袭能力;Western blot检测相关蛋白的表达。结果表明,干扰IscU2后,非小细胞肺癌细胞的增殖及克隆形成能力降低;细胞周期停滞在G1/G0期,同时伴随有p-AKT和Cyclin D1蛋白含量的下降;细胞晚期凋亡率明显增加,凋亡蛋白Cleaved-caspase3和Cleaved-PARP表达上调;细胞迁移和侵袭能力降低,上皮标志物E-Cadherin表达上调,间质标志物N-Cadherin和Snail表达下调;细胞ROS积累和线粒体膜电位下降。该研究结果表明,干扰IscU2显著抑制非小细胞肺癌的增殖、迁移、侵袭能力和上皮–间质转化,这为非小细胞肺癌的诊断和治疗提供了新的潜在靶点和视角。In this study,IscU2 was knocked down by shRNA interference technology in NSCLC NCI-H520 cell lines,and then we investigated the effects of IscU2 interference on cell proliferation,migration and invasion ability in NSCLC(non-small cell lung cancer)cells.The proliferation ability was detected by CCK-8 and colony formation assay.The changes of cell cycle,apoptosis,ROS and mitochondrial membrane potential were detected by flow cytometry.Transwell assay was used to detect cell migration and invision.Western blot was used to detect protein expression.The experiment results showed that when we inhibited the expression of IscU2 in NSCLC cells,the cell proliferation and colony formation ability were significantly lower than that of control group.Cell cycle was blocked at G1/G0 phase,and the expression of p-AKT and Cyclin D1 was downregulated.Meanwhile,the rate of late apoptosis was obviously increased,Cleaved-caspase3 and Cleaved-PARP,the key proteins of apoptosis were significantly upregulated.In addition,the cell migration and invision capacity were decreased,the epithelial marker E-Cadherin protein was increased and the mesenchymal markers,N-Cadherin and Snail proteins were reduced.Furthermore,it resulted in the accumulation of ROS and decreased the mitochondrial membrane potential.These results indicated that knockdown of IscU2 obviously inhibit the proliferation,migration and invision ability in NSCLC cells,which provide new potential targets and perspectives for treatment of non-small cell lung cancer.

关 键 词：非小细胞肺癌 IscU2 增殖 迁移 侵袭 

分 类 号：R734.2[医药卫生—肿瘤]