论文部分内容阅读
目的:研究干扰素-γ(Interferon-γ,IFN-γ)、干扰素-α2b(Interferon-α2b,IFN-α2b)二者联合应用对MCF-7乳腺癌细胞的诱导凋亡作用,并探讨其诱导凋亡作用的机制。方法:通过流式细胞仪(FCM)检测处理后细胞凋亡情况及Fas/FasL蛋白表达情况。结果:MCF-7乳腺癌细胞处理后凋亡细胞百分率增加,并且随着处理时间的延长,凋亡细胞百分率有增加趋势,差异显著,有统计学意义(p<0.05);FasL的表达增加,并且随着处理时间的延长,FasL的表达有增加趋势,差异显著,有统计学意义(p<0.05),Fas的表达实验组与对照组无明显变化,差异无统计学意义(p>0.05)。结论:干扰素-γ、干扰素-α2b二者联合应用可诱导MCF-7乳腺癌细胞凋亡,作用机制可能与通过上调FasL蛋白的表达,加强Fas/FasL之间的交联及使Fas/FasL通路敏感性增加有关。
Objective: To investigate the effect of Interferon-γ (IFN-γ) and Interferon-α2b (IFN-α2b) on the induction of apoptosis in MCF-7 breast cancer cells Mechanism of induction of apoptosis. Methods: Cell apoptosis and Fas / FasL protein expression were detected by flow cytometry (FCM). Results: The percentages of apoptotic cells increased after MCF-7 breast cancer cells were treated, and the percentage of apoptotic cells increased with the prolongation of treatment time (p <0.05); the expression of FasL increased, (P <0.05). There was no significant difference in the expression of Fas between the experimental group and the control group (p> 0.05), and there was no significant difference between the experimental group and the control group (P> 0.05) . Conclusion: The combination of interferon-γ and interferon-α2b could induce the apoptosis of MCF-7 breast cancer cells. The mechanism may be related to up-regulating the expression of FasL protein, enhancing the cross-linking between Fas / FasL and Fas / FasL pathway sensitivity increased.