中文摘要：

在人的某些癌症细胞中，组蛋白H3K27me3甲基化酶EZH2基因存在过表达的现象，很多研究已经证明，这可能是受MEK—ERK信号通路调控的．为了确定这种调控模式在小鼠细胞系中是否同样存在，以及MEK-ERK信号通路是否同时调控H3K27me3甲基化酶EZHl基因和去甲基化酶UTX、JMJD3基因的表达，用RT-PCR和Western印迹方法检测不同浓度的MEK-ERK抑制剂U0126（0、10、20、40μmol／L）对C2C12、C127、NIH3T3三种小鼠细胞系处理后，EZHl、EZH2基因和UTX、JMJD3基因表达变化．结果显示：MEK-ERK抑制剂处理后，3种细胞中EZHl和EZH2基因的表达与对照相比都有不同程度的降低，其中EZH2基因表达变化在C2C12、NIH3T3两种细胞达到显著水平（P〈0．05）．H3K27me3去甲基化酶UTX、JMJD3基因在3种细胞中表达均有升高，JMJD3升高达到显著水平（P〈0．05）．因此，在小鼠细胞系MEK-ERK信号通路可能参与调控EZH2、JMJD3基因的表达，但对EZHl、UTX基因的表达调控作用不明显．

英文摘要：

Many studies have shown that overexpression of H3K27 methylase gene EZH2 may be regulated by the MEK-ERK signaling pathway in some cancer cells. In order to determine whether it also exists in mice and the MEK-ERK signaling pathway could also involve the H3K27 methyltransferase gene EZHland H3K27 demethylase genes UTX and JMJD3, we used RT-PCR and Western blot methods to detect the expression of EZH1, EZH2, UTX and JMJD3 genes with the different concentrations of the MEK-ERK inhibitor U0126 （0, 10, 20, 40 p~mol/L） in three murine cell lines C2C12, C127 and NIH3T3. The results showed that the expression of H3K27 mehylase genes EZH1 and EZH2 decreased in the three cell lines compared with the control and the change of EZH2 gene expression reached the significant level （P 〈 0.05） in C2C12 and NIH3T3 two cell lines. The expression of UTX and JMJD3genes increased and that of JMJD3 gene reached the significant level （P 〈 0.05）. Therefore, in the murine cell lines the MEK-ERK signaling pathway may be involved in the regulation of EZH2 and JMJD3 genes, but the role on EZH1 and UTX genes is not obvious.