转录因子Foxp3对人肺腺癌细胞A549增殖周期的影响及机制研究  

Effect and mechanism of transcription factor Foxp3 on proliferation and cell cycle of human lung adenocarcinoma cell A549

作　　者：刘亚庆[1] 赵博[1] 罗亚东[1] 李祎南 杨巍[1] 

机构地区：[1]吉林大学基础医学院免疫学系,长春130021

出　　处：《中国免疫学杂志》2016年第4期490-494,共5页Chinese Journal of Immunology

摘　　要：目的:研究Foxp3对肺腺癌细胞A549增殖及细胞周期的影响,并探讨相关调控机制。方法:采用siRNA沉默A549细胞Foxp3表达;MTT法检测细胞增殖;流式细胞术检测细胞周期变化;RT-PCR筛选细胞周期相关checkpoint基因;免疫荧光及双荧光素酶报告基因分析Foxp3对相关checkpoint基因调控机制。结果:沉默A549细胞Foxp3后,其增殖明显减慢并发生G_0/G_1期阻滞,G_1/S期checkpoint基因CCND1表达显著降低。机制研究发现Foxp3能直接调控CCND1表达。结论:Foxp3通过上调细胞周期G_1/S期checkpoint基因CCND1表达,促进肺腺癌细胞A549增殖,从而促进了肺腺癌发展,为肺腺癌的发生发展及治疗靶点提供了新思路。Objective： To investigate the effect and mechanism of transcription factor Foxp3 on the proliferation and cell cycle of human lung adenocarcinoma cell line A549. Methods： We knocked down the expression of Foxp3 using siRNA. Foxp3 inhibition was detected by RT-PCR. Cell proliferation was detected by MTT. Cell cycle of A549 cells were detected by flow cytometry after the transfection of siRNA. Cell cycle-related checkpoint genes were filtered by RT-PCR. The regulation of Foxp3 on cell cycle-related checkpoint genes were detected by immunofluorescence and dual-luciferase reporter assay system. Results： The proliferation of A549 cells were inhibited after silencing Foxp3,and A549 cells were arrested in G0/ G1 cycle. G1/ S cycle checkpoint gene CCND1 was down regulated. Mechanism research show that Foxp3 can regulate the expression of CCND1 directly. Conclusion： Foxp3 can promote the proliferation of A549 cell line by up regulating G1/ S cycle checkpoint gene CCND1. This provides a new target for the therapeutic targets of lung adenocarcinoma.

关 键 词：FOXP3 CCND1 肺腺癌 增殖 细胞周期 

分 类 号：R730.3[医药卫生—肿瘤]