Janus激酶/信号传导子和转录激活子信号通路重建对MHCC97细胞干扰素α应答的影响

目的阐明原发性肝癌MHCC97细胞中Janus激酶/信号传导子和转录激活子信号通路对干扰素α抗肿瘤增殖作用的影响.方法用Dosper转染干扰素调节因子9（IRF9）表达质粒入MHCC97细胞;用Western blot和寡核苷酸迁移率实验分别检测肝癌细胞中IRF9、细胞周期调控蛋白和干扰素刺激基因因子3的表达;用四甲基偶氮唑盐和流式细胞术分别检测细胞的增殖水平及各期细胞的分布情况. 结果通过高表达IRF9因子可恢复MHCC97细胞对干扰素α抗增殖的应答能力,同时阻滞细胞由S期过渡到G 2期.结论完整的Janus激酶/信号传导子和转录激活子信号通路对介导干扰素α抗肝癌MHCC97细胞的增殖作用至关重要.

Reconstructing the JAK/STATs signal pathway restored the anti-proliferative response of MHCC97 on interferon alpha

Objective To elucidate the roles of JAK/STATs signal pathway on anti-proliferative effects induced by IFN-aipha in MHCC97. Methods An IRF9 expression vector was transfected into MHCC97 with Dosper. The expression of IRF9, cycle regulating proteins and the forming of ISGF3 complex were detected using Western blot and EMSA, respectively. Cell proliferation and distribution were monitored using MTT and flow cytometry. Results High expression of IRF9 restored the anti-proliferative response of MHCC97 on IFN-aipha treatment and delayed the cell transition from S phase to G2 phase induced by IFN-aipha. Conclusion The integrity and functions of JAK/STATs signal pathway played an important role in mediating the anti-proliferative effects of IFN-aipha in MHCC97,