Analysis of signal transduction in human glioma cells transfected with cytokine gene

我们的目的是分析细胞因子基因转染人脑胶质瘤细胞诱导的抗肿瘤活性的机制，为了阐明对细胞因子敏感性不同的潜在机制，我们检测了当外源性细胞因子（干扰素-β（IFN-β）或肿瘤坏死因子-α（TNF-α））加入人脑胶质瘤细胞时，磷酸化或NF-κ B复合物的程度。这些结果表明，不同的NF-κ B复合物的细胞因子诱导的人脑胶质瘤细胞可能与肿瘤细胞对细胞因子的不同程度的敏感性。为了阐明细胞因子基因转染的抗肿瘤活性的机制，我们在视频增强对比微分干涉相差显微镜下观察形态学变化。携带核内人IFN-β基因的细胞经历了以流血的形成和细胞质沸腾为特征的形态学变化，例如凋亡。在C57 BL/6小鼠的体内实验中，我们证实了当将含有小鼠IFN-β基因的脂质体注射到实验性胶质瘤中时，细胞免疫的激活。

Our aim is analysis of mechanisms of antitumor activity induced by cytokine gene transfection into human glioma cells.To clarify the underlying mechanisms involved in the different susceptibility to cytokines, we examined the degrees of phosphorylation or NF-kappaB complex when cytokines (interferon-beta (IFN-beta) or tumor necrosis factor-alpha (TNF-alpha)) were exogenously added to human glioma cells. These results suggest that the different NF-kB complex induced by cytokines in human glioma cells might be related to the varying degrees of susceptibility of tumor cells to cytokines.To elucidate the mechanisms underlying the antitumor activity of cytokine gene transfection using cationic liposomes, we observed morphological changes under video-enhanced contrast differential interference contrast microscopy. Cells harboring the intranuclear human IFN-beta gene underwent morphological changes characterized by bled formation and cytoplasmic boiling such as apoptosis. On the other hand, exogenously added cytokines did not induce the changes at all.In in vivo experiments using C57BL/6 mouse, we confirmed the activation of cellular immunity when liposomes, containing mouse IFN-beta gene were injected into the experimental glioma.