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目的:通过Vk3诱导人宫颈癌Hela细胞损伤,观察Hela细胞Notch-1、Notch-2及其配体Jagged-1、Jagged-2,细胞周期素D1(Cyclin D1)mRNA表达的变化及N-乙酰半胱氨酸(NAC)对其的影响,探讨Notch在人宫颈癌发生发展过程中的作用。方法:实验分组为对照组、Vk3处理(Vk3)组、Vk3与NAC联合作用(Vk3+NAC)组及NAC单独应用(NAC)组,用RT-PCR方法检测Hela细胞中Notch-1、Notch-2、Jagged-1、Jagged-2及Cyclin D1 mRNA表达的变化。结果:与对照组相比,Vk3组Notch-1、Notch-2、Jagged-1、Jagged-2及Cyclin D1 mRNA表达明显下降,而Vk3+NAC组明显高于Vk3组(P<0.05)。结论:Vk3诱导人宫颈癌Hela细胞损伤,降低了Notch-1、Notch-2、Jagged-1、Jagged-2及Cyclin D1 mRNA的表达,NAC增加了Hela细胞Notch-1、Notch-2、Jagged-1、Jagged-2及Cyclin D1 mRNA的表达而减轻了Hela细胞损伤,表明Notch信号通路参与了人宫颈癌的发生。
OBJECTIVE: To observe the changes of mRNA expression of Notch-1, Notch-2 and its ligand Jagged-1, Jagged-2 and Cyclin D1 in Hela cells by Vk3-induced Hela cell injury and N-acetyl Cysteine (NAC) on the impact of Notch on the development of human cervical cancer in the process. Methods: The experimental groups were divided into control group, Vk3 treatment group (Vk3), Vk3 + NAC combined group and NAC alone group (NAC) group. The expressions of Notch- 2, Jagged-1, Jagged-2 and Cyclin D1 mRNA expression changes. Results: Compared with the control group, the mRNA expression of Notch-1, Notch-2, Jagged-1, Jagged-2 and Cyclin D1 in Vk3 group was significantly lower than that in Vk3 + NAC group (P <0.05). Conclusion: Vk3 can induce the injury of Hela cells and decrease the mRNA expression of Notch-1, Notch-2, Jagged-1, Jagged-2 and Cyclin D1 in Hela cells. NAC increases the expression of Notch-1, Notch- 1, Jagged-2 and Cyclin D1 mRNA expression and reduce Hela cell injury, indicating that Notch signaling pathway involved in the occurrence of human cervical cancer.