文章摘要
徐 然,仇文进,陈正新,冯 爽,蔡小敏,王慧博,刘 宁.FOXP2调控PI3K/Akt信号通路抑制胶质瘤的侵袭[J].南京医科大学学报,2017,(5):559~563
FOXP2调控PI3K/Akt信号通路抑制胶质瘤的侵袭
FOXP2 inhibits GBM cell invasion and migration through regulating PI3K/Akt pathway
投稿时间:2017-01-13  
DOI:10.7655/NYDXBNS20170508
中文关键词: 胶质瘤;FOXP2  PI3K/Akt;侵袭;迁移
英文关键词: GBM  FOXP2  PI3K/Akt  invasion  migration
基金项目:国家自然科学基金(81201978);江苏省科技厅基础研究计划(BK2012483)
作者单位
徐 然 南京医科大学第一附属医院神经外科江苏 南京 210029 
仇文进 南京医科大学第一附属医院神经外科江苏 南京 210029 
陈正新 南京医科大学第一附属医院神经外科江苏 南京 210029 
冯 爽 南京医科大学第一附属医院神经外科江苏 南京 210029 
蔡小敏 南京医科大学第一附属医院神经外科江苏 南京 210029 
王慧博 南京医科大学第一附属医院神经外科江苏 南京 210029 
刘 宁 南京医科大学第一附属医院神经外科江苏 南京 210029 
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中文摘要:
      目的:探讨叉头框P2基因(FOXP2)对胶质细胞瘤细胞侵袭的影响。方法:采用荧光定量PCR技术与Western blot分别检测FOXP2在正常星型胶质细胞与胶质瘤细胞中的核糖核酸与蛋白表达水平。用携带FOXP2基因慢病毒质粒转染胶质瘤细胞U87和U251细胞系,通过划痕实验、Transwell侵袭实验和Western blot观察其对胶质瘤细胞侵袭性以及PI3K、Akt蛋白的影响。结果:FOXP2的表达在胶质瘤细胞U87和U251中明显低于正常星型胶质细胞。上调FOXP2后,胶质瘤细胞U87和U251细胞侵袭性明显降低,Akt与PI3K表达明显降低。结论:FOXP2通过调控PI3K/Akt通路可以在一定程度上抑制胶质瘤细胞的侵袭能力,从而延缓胶质瘤的发生发展。
英文摘要:
      Objective:To explore Forkhead box P2 (FOXP2) expression in GBM cell and its effect on invasion and migration of U87 and U251 GBM cells. Methods:RT-qPCR and Western blot were used to detect the mRNA and protein levels of FOXP2 in NHA and GBM cells. pEGFP-FOXP2 was constructed according to the manufacturer’s instructions and transfected into U87 and U251 cells. Wound healing assay and Transwell assay were used to test the invasion and migration ability of GBM cells. The changes of PI3K, Akt proteins was detected by Western blot. Results:The expression of FOXP2 was decreased in GBM cells both in mRNA and protein levels. The overexpression of FOXP2 significantly decreased the ability of invasion and migration of GBM cells and reduced the expression of PI3K and Akt proteins. Conclusion:FOXP2 is reduced in GBM cells and upregulating FOXP2 could increase invasion and migration of GBM cells through PI3K/Akt pathway, indicating that FOXP2 may serve as a tumor suppresser,which inhibits invasion of tumor cells during the development of GBM.
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