临床神经外科杂志2017，Vol.14Issue(1)：21-25,5.DOI:10.3969/j.issn.1672-7770.2017.01.006
FRK 通过调节 EGFR-Y1173磷酸化促进脑胶质瘤细胞凋亡作用的研究
FRK promotes the apoptosis of glioma cells by regulating phosphorylation of EGFR-Y1173
摘要
Abstract
Objective To study whether FRK can promote the apoptosis of glioma cells by regulating phosphorylation of EGFR-Y1173.Methods The FRK plasmid was transfected into glioma U251 cells,transfection efficiency ,the protein level and Y1173 phosphorylation of EGFR was exmined by western blot .The flow cytometry was used to examine the apoptosis of glioma cells .The EGFR(WT) and EGFR(Y1173F) plasmids were transfected to glioma U251 cells respectively,also the FRK,EGFR( WT) and EGFR( Y1173F) were co-transfected to glioma U251 cells,the apoptosis of glioma cells was tested by flow cytometry .Results The FRK plasmid was transfected into glioma U251 cells successfully ,FRK over-expression promoted the apoptosis of glioma U 251 cells.And FRK over-expression increased the EGFR-Y1173 phosphorylation ,but had no effect on the protein level of EGFR.Also, the ability of glioma cells apoptosis was all decreased in EGFR ( WT ) and EGFR ( Y1173 F ) over-expression group , and decreased by 25% and 75%, respectively .WB results showed,the FRK,EGFR(WT) and EGFR(Y1173F) plasmid were co-transfected into glioma U251 cells successfully .The flow cytometry results showed , the ability of glioma cells apoptosis was increased after FRK over-expression,but decreased in EGFR overexpression group ,and the effect of EGFR(Y1173F) on glioma cells apoptosis showed stronger than EGFR (WT)'s.In addition,the promoting effect of FRK on glioma cells apoptosis was abolished after EGFR ( Y1173F) plasmid transfection .Conclusion FRK can regulate the glioma cells apoptosis by promoting phosphorylation of EGFR-Y1173 .关键词
胶质瘤/FRK/EGFR/凋亡Key words
glioma/FRK/EGFR/apoptosis分类
医药卫生引用本文复制引用
张道为,于如同,石琼,金戈,王军,宋旭,蔡畅,方震,周秀萍,郭克勤..FRK 通过调节 EGFR-Y1173磷酸化促进脑胶质瘤细胞凋亡作用的研究[J].临床神经外科杂志,2017,14(1):21-25,5.基金项目
国家自然科学基金（81372699，81472345，81402046）；江苏省普通高校研究生科研创新计划项目 （）
