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目的探讨整合素αvβ3在IGF-II诱导的宫颈癌细胞株增殖中的作用。方法用MTT法观察细胞增殖,用Western blot测定细胞ERK1/2(p42/44MAPK)磷酸化表达。结果用IGF-IR单克隆抗体(1,5,10μmol/L)和αvβ3单克隆抗体(10,15,20μmol/L)预处理30分钟可显著抑制IGF-II(20 ng/ml)诱导的SiHa细胞增殖,并呈剂量依赖性。IGF-II(100 ng/ml)可诱导SiHa细胞p42/44MAPK磷酸化表达,IGF-IR(10μmol/L)及αvβ3(15μmol/L)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,整合素αvβ3与IGF-IR信号通路上存在着交互作用。
Objective To investigate the role of integrin αvβ3 in the proliferation of cervical cancer cell lines induced by IGF-II. Methods Cell proliferation was observed by MTT assay. The phosphorylation of ERK1 / 2 (p42 / 44 MAPK) was detected by Western blot. Results Pretreatment with IGF-IR monoclonal antibody (1,5,10μmol / L) and αvβ3 monoclonal antibody (10,15,20μmol / L) for 30min significantly inhibited the proliferation of SiHa induced by IGF- Cells proliferated in a dose-dependent manner. IGF-II (100 ng / ml) could induce p42 / 44 MAPK phosphorylation in SiHa cells. Monoclonal antibodies with IGF-IR (10 μmol / L) and αvβ3 (15 μmol / L) significantly inhibited p42 / 44MAPK phosphorylation. Conclusion IGF-II can activate the p42 / 44MAPK signaling pathway in SiHa cell line, and integrin αvβ3 interacts with IGF-IR signaling pathway.