Effect of the expression of CENPⅠon the biological function of lung adenocarcinoma H1650 cells and its mechanism
10.12007/j.issn.0258-4646.2025.05.009
- VernacularTitle:CENPⅠ对肺腺癌H1650细胞生物学功能的影响及其机制
- Author:
Xiaotian LI
1
;
Qifei WU
;
Huijie HE
;
Haiying NIU
;
Jingyi LIU
;
Dong ZHANG
Author Information
1. 内蒙古科技大学包头医学院 第一附属医院呼吸与危重症医学科,内蒙古 包头 014040;内蒙古科技大学包头医学院 研究生院,内蒙古 包头 014040
- Publication Type:Journal Article
- Keywords:
lung adenocarcinoma;
centromere proteinⅠ;
epithelial-mesenchymal transition;
PI3K/AKT/MTOR signaling pathway
- From:
Journal of China Medical University
2025;54(5):431-436
- CountryChina
- Language:Chinese
-
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.
