论文部分内容阅读
为探讨IL 6促进 7TD1细胞增殖的机制 ,本研究采用凝胶阻滞电泳方法比较IL 6对核因子STAT3(代表JAK STATs通路 )、NF IL 6 (代表Ras/MAPK/NF IL 6通路 )的激活方式 ,以反义寡核苷酸 (ASODNs)阻断IL 6对核因子的激活 ,检测ASODNs对IL 6效应的影响 ,并采用MEK特异性抑制剂PD0 980 5 9阻断Ras/MAPK通路的激活 ,观测Ras/MAPK通路的功能意义。结果发现STAT3与NF IL 6都可被低剂量IL 6激活 ,但NF IL 6激活后持续的时间比STAT3长。STAT3ASODN对IL 6效应的影响很弱 ,而NF IL 6ASODN可显著拮抗IL 6的促增殖作用。PD0 980 5 9的作用同NF IL 6ASODN相似。这些结果说明在 7TD1细胞中 ,Ras/MAPK/NF IL 6途径介导IL 6的促增殖信号。
In order to investigate the mechanism of IL-6 promoting proliferation of 7TD1 cells, we used gel-block electrophoresis to compare the effects of IL-6 on nuclear factor STAT3 (representing JAK STATs pathway) and NF IL6 (representing Ras / MAPK / NF IL6 pathway) Way, antisense oligonucleotides (ASODNs) were used to block the activation of nuclear factor 6 (IL-6) and the effect of ASODNs on IL-6, and the activation of Ras / MAPK pathway was blocked by MEK specific inhibitor PD0 98059 , To observe the functional significance of Ras / MAPK pathway. The results showed that STAT3 and NF IL6 can be activated by low dose of IL6, but NF IL6 activation lasting longer than STAT3. STAT3ASODN had a weaker effect on IL6 effect, while NF IL6ASODN significantly inhibited the effect of IL6 on proliferation. The effect of PD0 980 5 9 is similar to that of NF IL 6 ASODN. These results indicate that the Ras / MAPK / NF IL6 pathway mediates the pro-proliferative signal of IL6 in 7TD1 cells.