南京医科大学学报（自然科学版）2017，Vol.37Issue(5)：559-563,5.DOI:10.7655/NYDXBNS20170508
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
摘要
Abstract
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.关键词
胶质瘤/FOXP2/PI3K/Akt/侵袭/迁移Key words
GBM/FOXP2/PI3K/Akt/invasion/migration分类
医药卫生引用本文复制引用
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（自然科学版）,2017,37(5):559-563,5.基金项目
国家自然科学基金(81201978) （81201978）
江苏省科技厅基础研究计划(BK2012483) （BK2012483）
