摘要
目的探讨胰岛素样生长因子Ⅱ(IGF-Ⅱ)激活宫颈癌SiHa细胞株ERK1/2(p42/44MAPK)信号通路的模式变化及对其增殖的影响。方法用MTT法观察细胞增殖,用Westernblot测定细胞p42/44MAPK磷酸化表达。结果IGF-Ⅱ可诱导SiHa细胞增殖,并呈剂量依赖性;用IGF-IR单克隆抗体(1,5,10μmol/L)预处理30min可显著抑制IGF-Ⅱ(20ng/mL)诱导的SiHa细胞增殖,并呈剂量依赖性。IGF-II(100ng/mL)可诱导SiHa细胞p42/44MAPK磷酸化表达,20min达到高峰;IGF-IR单克隆抗体可显著抑制IGF-Ⅱ诱导的Siha细胞p42/44MAPK磷酸化。结论IGF-II可激活宫颈癌SiHa细胞株p42/44MAPK信号通路,并可能通过p42/44MAPK信号通路调控SiHa细胞增殖。
[Objective] To investigate the changes of p42/44 mitogen-activated protein kinase （p42/44MAPK） phosphorylation induced by insulin-like growth factor Ⅱ（IGF-Ⅱ） in cervical cancer SiHa cell line, and also to detect the effect of IGF-Ⅱ on cervical cancer SiHa cells proliferation. [Methods] MTT was used for examining the cell proliferation. Western blot was used for examining the p42/44MAPK phosphorylation. [Results] IGF-Ⅱ increased the cervical cancer SiHa cell proliferation in vitro, and pretreatment of anti-IGF-IR monoclonal antibody（1, 5, 10 μmol/L）for30 min reduced the cell proliferation induced by IGF-Ⅱ （20 ng/mL） in a dose-dependent manner. Following excitation by IGF-Ⅱ （100 ng/mL） in vitro, there was substantial up-regulation of p42/44MAPK phosphorylation in cervical cancer SiHa cells with maximal activation at 20 rain. Pre-treatment with anti-IGF-IR monoclonal antibody（ 10 μmol/L） in SiHa cells before IGF-II was used, and the expression of p42/44MAPK phophorylation was inhibited markedly. [Conclusions] IGF-Ⅱ may induce phosphorylation of p42/44MAPK in cervical cancer SiHa cell line, and the activation of p42/44MAPK may regulate the proliferation of SiHa cell line.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2007年第20期2445-2448,共4页
China Journal of Modern Medicine
基金
黑龙江省科技厅基金资助(编号:LC02C17)
