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目的:探讨Cyclin D2、Cyclin E和p27在慢性粒细胞性白血病(CML)发病过程中的作用机制。方法:以RT-PCR和FCM方法分别检测CML患者白血病细胞和K562细胞中Cyclin D2、Cyclin E和p27 mRNA的表达及细胞周期分布情况,并以正常人骨髓单个核细胞做对照分析。结果:与对照组相比CML患者白血病细胞和K562细胞中Cyclin D2 mRNA的表达增高,tCML=2.842,PCML<0.01;tK562=2.908,PK562<0.01。Cyclin E mRNA的表达也增高,tCML=2.109,PCML<0.05;tK562=2.193,PK562<0.05。p27 mRNA的表达降低,tCML=2.688,PCML<0.01;tK562=2.357,PK562<0.05。G0/G1期细胞减少(tCML=2.386,PCML<0.05;tK562=2.408,PK562<0.05),而S期细胞增多(tCML=2.114,PCML<0.05;tK562=2.203,PK562<0.05)。结论:Cyclin D2、Cyclin E和p27 mRNA的表达在CML中发生了明显改变,致使G0/G1期缩短,细胞快速通过G1/S转换点进入S期,加速细胞周期进程和细胞增殖,导致CML的发生。
Objective: To explore the mechanism of Cyclin D2, Cyclin E and p27 in the pathogenesis of chronic myeloid leukemia (CML). Methods: The expressions of Cyclin D2, Cyclin E and p27 mRNA in CML patients and K562 cells were detected by RT-PCR and FCM respectively. The normal human bone marrow mononuclear cells were used as controls. Results: Compared with the control group, the expression of Cyclin D2 mRNA in leukemia cells and K562 cells in CML patients was increased, tCML = 2.842, PCML <0.01; tK562 = 2.908, PK562 <0.01. Cyclin E mRNA expression also increased, tCML = 2.109, PCML <0.05; tK562 = 2.193, PK562 <0.05. p27 mRNA expression decreased, tCML = 2.688, PCML <0.01; tK562 = 2.357, PK562 <0.05. The number of cells in G0 / G1 phase decreased (tCML = 2.386, PCML <0.05; tK562 = 2.408, PK562 <0.05), but increased in S phase (tCML = 2.114, PCML <0.05; tK562 = 2.203, PK562 <0.05). CONCLUSIONS: The expressions of Cyclin D2, Cyclin E and p27 mRNA are significantly changed in CML, resulting in the shortening of G0 / G1 phase. The cells rapidly enter the S phase through the G1 / S transition point, accelerating cell cycle progression and cell proliferation, occur.