p38MAPK信号转导通路在EGF诱导食管腺癌SEG-1细胞表达u-PA中的作用  

Role of the p38MAPK signaling pathway in EGF-induced u-PA expression in esophageal adenocarcinoma SEG-1 cells

作　　者：李宁[1] 陈娟[1] 白研[2] 白文元[1] 

机构地区：[1]河北医科大学第二医院消化内科,河北省石家庄市050000 [2]河北医科大学第三医院,河北省石家庄市050000

出　　处：《世界华人消化杂志》2012年第16期1458-1462,共5页World Chinese Journal of Digestology

基　　金：河北省自然科学基金资助项目;No.C2008001083~~

摘　　要：目的:探讨表皮生长因子(epidermal growth factor,EGF)对人食管腺癌SEG-1细胞尿激酶型纤溶酶原激活物(urokinase-type plasminogen activator,u-PA)mRNA和蛋白表达的影响及p38MAPK信号转导通路在其中的作用.方法:以相同浓度的EGF(100g/L)按时间梯度刺激SEG-1细胞,应用Western blot法测定各时间点总p38MAPK蛋白、磷酸化p38MAPK蛋白、u-PA蛋白表达,并应用RT-PCR方法检测各时间点u-PAmRNA表达.用p38MAPK特异抑制剂SB203580预处理细胞后,观察上述指标变化.结果:EGF可明显增强SEG-1细胞(u-PA)mRNA和蛋白的表达,并可激活p38MAPK蛋白的磷酸化,具有时间依赖性.SB203580能明显抑制EGF诱导的p38MAPK蛋白的磷酸化,用其阻断p38MAPK信号转导通路后,EGF对u-PAmRNA和蛋白表达的诱导作用受到显著抑制,并且具有剂量依赖性.结论:EGF可通过p38MAPK信号转导通路诱导SEG-1细胞表达u-PA.AIM： To study the effect of epidermal growth factor （EGF） on the mRNA and protein expression of urokinase-type plasminogen activator （u-PA） in esophageal adenocarcinoma SEG-1 cells and to detect the role of the p38MAPK signaling pathway in this process. METHODS： After SEG-1 cells non-pre-incubated or pre-incubated with SB203580 （a p38MAPK inhibitor） for two hours were treated with EGF （100 g/L） for different durations, the protein expression of total p38MAPK, phosphorylated p38MAPK and u-PA was determined by Western blot, and the expression of u-PA mRNA was examined by reverse transcription-polymerase chain reaction （RT-PCR）. RESULTS： Treatment with EGF significantly increased the mRNA and protein expressions of u-PA and induced p38 kinase phosphorylation in SEG-1 cells in a time-dependent manner. SB203580 could sufficiently suppress EGF-induced p38MAPK phosphorylation and significantly attenuate EGF-induced u-PA mRNA and protein expression in SEG-1 cells in a dosedependent manner. CONCLUSION： EGF can significantly induce u-PA in SEG-1 cells by activating the p38MAPK signaling pathway.

关 键 词：表皮生长因子 P38丝裂原活化蛋白激酶 尿激酶型纤溶酶原激活物 肿瘤细胞侵袭 

分 类 号：R735.1[医药卫生—肿瘤]