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研究EBV体外再感染CNE-2Z细胞后,不同组分中PKC(蛋白激酶C)和TPK(酪氨酸蛋白激酶)活性的影响,并探讨PKC和TPK活性与细胞增殖的关系。实验分三组即对照组、EBV组和EBV+TPA组,用免疫细胞化学(以小鼠抗EB病毒早期抗原)检测EBV在体外能否再感染CNE-2Z细胞,用特异底物法和特异激活剂法分别测定其PKC和TPK活性,MTT法检测CNE-2Z细胞体外增殖能力。结果显示未处理CNE-2Z细胞中PKC活性为膜性>胞 核>胞液,TPK为胞核>膜性>胞液。EBV和EBV+TPA再感染CNE-2Z细胞后,抑制细胞增殖,同时胞液PKC和TPK活性升高,膜性和胞核TPK和膜性PKC活性降低。本研究结果提示,EBV可能通过影响不同细胞组分中PKC和 TPK活性来调节CNE-2Z鼻咽癌细胞的增殖。
To study the effect of PKC (PKC) and TPK (tyrosine protein kinase) on the activity of EBV in vitro re-infected CNE-2Z cells and to explore the relationship between PKC and TPK activity and cell proliferation. EBV group and EBV + TPA group were divided into three groups: control group, EBV + TPA group and immunocytochemistry (early mouse anti-Epstein-Barr virus) to detect whether EBV could infect CNE-2Z cells in vitro. Activator method were measured PKC and TPK activity, MTT assay CNE-2Z cell proliferation in vitro. The results showed that PKC activity in untreated CNE-2Z cells was membranous> cytoplasm> cytokines and TPK was> nuclear> membranous> cytosol. After re-infection with EBV and EBV + TPA, the proliferation of CNE-2Z cells was inhibited. Meanwhile, the activities of PKC and TPK in the cytoplasm increased, while the activities of TPK and membrane PKC decreased. The results of this study suggest that EBV may regulate the proliferation of CNE-2Z nasopharyngeal carcinoma cells by affecting PKC and TPK activities in different cell components.