中国医科大学学报2025，Vol.54Issue(5)：431-436,6.DOI:10.12007/j.issn.0258-4646.2025.05.009
CENPⅠ对肺腺癌H1650细胞生物学功能的影响及其机制
Effect of the expression of CENPⅠon the biological function of lung adenocarcinoma H1650 cells and its mechanism
摘要
Abstract
Objective To investigate the expression level of centromere protein(CENP)Ⅰin lung adenocarcinoma cells,to study the effects of CENPⅠon the proliferation,invasion,migration,apoptosis,and epithelial-mesenchymal transition(EMT)of lung adenocarci-noma cells,and to explore the possible mechanisms related to its occurrence.Methods The expression of CENPⅠmRNA and protein in four types of lung adenocarcinoma cells and normal alveolar epithelial cells were detected by quantitative real-time polymerase chain reaction(RT-qPCR)and Western blotting.The expression of CENPⅠin H1650 cells was knocked down by the siRNA technique,The transfection efficiency was detected by RT-qPCR and Western blotting.The effects of knock-down CENPⅠon proliferation,cell cycle,apoptosis,invasion and migration of H1650 cells were detected by the cell counting kit-8 assay,the transwell assay,and flow cytometry.Western blotting was used to detect the expression of E-cadherin,N-cadherin,vimentin,Ki-67,cyclin D1,Bcl-2,PI3K,AKT,mTOR,p-PI3K,p-AKT,and p-mTOR.Results After the knock-down of CENPⅠ,the proliferative ability of the H1650 cells significantly decreased,the number of apoptotic cells significantly decreased,and the cell invasion and migration abilities significantly decreased(P<0.01).E-cadherin expression was upregulated and N-cadherin,vimentin,Ki-67,cyclin D1,Bcl-2,p-PI3K,p-AKT,and p-mTOR expres-sion were down-regulated in the CENTI group compared with the control group(P<0.05).The expression of p-PI3K,p-AKT,and p-mTOR in the si-CENPⅠ+IGF-1 group was upregulated compared to that in the si-CENPⅠgroup(P<0.05).Conclusion High expression of CENPⅠin lung adenocarcinoma cells promotes the proliferation,invasion,and migration of lung adenocarcinoma H1650 cells and EMT inhibits apoptosis,which may be related to the activation of the PI3K/AKT/mTOR signaling pathway.关键词
肺腺癌/人着丝粒蛋白Ⅰ/上皮-间质转化/PI3K/AKT/mTOR信号通路Key words
lung adenocarcinoma/centromere proteinⅠ/epithelial-mesenchymal transition/PI3K/AKT/MTOR signaling pathway分类
医药卫生引用本文复制引用
李晓甜,吴启飞,何慧洁,牛海英,刘静怡,张冬..CENPⅠ对肺腺癌H1650细胞生物学功能的影响及其机制[J].中国医科大学学报,2025,54(5):431-436,6.基金项目
内蒙古医学科学院公立医院科研联合基金科技项目(2023GLLH0206) （2023GLLH0206）
包头市卫生健康科技计划(wsjkkj009) （wsjkkj009）
