JNK MAPK信号通路在食管癌细胞系Eca-109细胞中的作用机制

Mechanism of JNK1/2 MAPK signaling pathway in human esophageal cancer cell line Eca-109

目的探讨c-jun氨基末端激酶1/2(c-jun N-teuninal kinase,JNK 1/2)信号通路在食管癌细胞系Eca-109细胞中的作用。方法体外培养Eca-109细胞,以特异性JNK信号转导通路抑制剂SP600125处理Eca-109细胞;RT-PCR的方法检测JNK1和JNK2基因的表达,Western blot法检测JNK和p-JNK蛋白的表达,MTT(3-(4,5-Dimethylthiazol-2-yl)-2,5-di-phenyltetrazolium bromide)法检测细胞增殖,流式细胞术检测细胞凋亡。结果 Eca-109细胞经SP600125分别处理24h和48 h后,分别与对照组比较,JNK1 mRNA的表达无统计学差异(均P>0.05),JNK2 mRNA的表达也无统计学差异(均P>0.05),但活化的JNK即P-JNK1/2蛋白的表达显著减少,细胞的增殖显著被抑制,细胞的凋亡率有统计学差异(均P<0.05)。结论 JNK信号通路可能在Eca-109细胞的发生发展中发挥重要作用。

Objective To explore mechanism of c-Jun N-teuninal kinase（JNK1/2） signaling pathway in human esophageal cancer cell line Eca-109.Methods Eca-109 cells were cultured in vitro and then treated with SP600125,a specific JNK inhibitor,and mRNA expression of JNK1/2 was examined by RT-PCR;the expression of p-JNK protein was detected by western blot.MTT was used to perform cell growth inhibitory rate.Flow cytometry was taken to evaluate apoptosis at a very early stage.Results After being treated by SP600125 with 24 h and 48 h,the mRNA expression of JNK1 displayed no statistical significance（both P0.05）,the mRNA expression of JNK2 showed no statistical significance（both P0.05）;but protein expression of p-JNK1/2 was remarkably reduced by SP600125 as well as the apoptosis rate and cell growth inhibitory rate in the human esophageal cancer cell line Eca-109 cells as compared with control group（both P0.05）.Conclusions JNK signaling pathway may play an important role in the carcinogenesis of Eca-109 cells.