摘要
目的探讨B7H3和纤维连接蛋白(FN)相互作用对人慢性髓性白血病细胞系K562细胞凋亡的影响。方法采用流式细胞术检测K562细胞中B7H3分子的表达,构建B7H3过表达细胞采用免疫共沉淀技术检测B7H3与FN的相互作用。添加外源FN后,通过细胞实验检测细胞黏附和细胞凋亡的变化。Western blot法检测凋亡相关蛋白及PI3K/AKT信号通路的变化。结果①K562细胞低表达B7H3分子.慢病毒转染后得到稳定表达B7H3的细胞系K562 OE-B7H3及其对照细胞系K562NC-B7H3细胞。②B7H3与FN之间存在相互作用(P=0.036)。③B7H3与FN的相互作用促进细胞黏附(P<0.05),抑制细胞凋亡(P<0.05)。④B7H3与FN相互作用激活PI3K/AKT信号通路(P<0.05)结论B7H3与FN相互作用促进了细胞黏附,可能通过激活PI3K/AKT信号通路抑制K562细胞的凋亡。
Objective To explore the effect of the interaction between B7H3 and fibronectin(FN)on the apoptosis of human chronic myeloid leukemia K562 cells.Methods The expression of B7H3molecules in K562 cells was detected using flow cytometry and B7H3 overexpressing cells wereconstructed.The interaction between B7H3 and FN was detected using the co-immunoprecipitationtechnology.After adding exogenous FN,cell experiments were performed to detect changes in adhesionand cell apoptosis.The changes in apoptosis-related proteins and PI3K/AKT signaling pathway weredetected using Western blot.Results The expression of B7H3 was low in K562,and the cell line K562OE(overexpression)-B7H3 and the control cell line K562 NC(negative control)-B7H3 were obtainedafter lentivirus transfection.There is an interaction between B7H3 and FN(P=0.036),and this interactionpromoted cell adhesion(P<0.05),inhibited cell apoptosis(P<0.05),and activated the PI3K/AKTsignaling pathway(P<0.05).Conclusion B7H3 interacts with FN to promote cell adhesion and mayinhibit K562 cell apoptosis by activating the Pl3K/AKT signaling pathway.
作者
孙美云
谢金晶
张东泽
张光波
Sun Meivun;Xie Jinjing;Zhang Dongze;Zhang Guangbo(Department of Medicine,Soochow University,Suzhou 216007,China;Jiamgsu Key Laboratory of Clinical Immunology,Suzhou 216007,China;The First Affiliated Hospital of Soochow University,Suzhou 216007,China)
出处
《中华血液学杂志》
CAS
CSCD
北大核心
2021年第11期939-944,共6页
Chinese Journal of Hematology
基金
国家自然科学基金面上项目(81872328)。
