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本研究探讨ERK和P38信号转导途径对慢性髓系白血病(CML)细胞周期的调控作用。以RT-PCR、Western blot和FCM方法分别检测CML患者白血病细胞和K562细胞中ERK、p38、cyclin D2、cyclin E、p27的mRNA表达及蛋白表达(其中ERK和P38为磷酸化ERK和磷酸化P38)及细胞周期分布,并分析其相关关系。结果表明:CML患者白血病细胞和K562细胞中ERK、P38、cyclin D2、cyclin E的mRNA表达和蛋白表达增高,P27的表达降低,且cyclin D2蛋白表达与cyclin E、ERK和P38蛋白表达呈正相关(P<0.01),与P27蛋白表达呈负相关(P<0.01)。G0/G1期细胞减少,S期细胞增多,与对照组相比有显著性差异。结论:CML中P38、ERK mRNA表达和活性增加,激活下游的cyclin D2、cyclin E和P27等细胞周期调控因子,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。
This study was aimed to investigate the role of ERK and P38 signal transduction in the regulation of cell cycle in chronic myeloid leukemia (CML). The mRNA and protein expressions of ERK, p38, cyclin D2, cyclin E, p27 in CML patients and leukemia cells and K562 cells were detected by RT-PCR, Western blot and FCM respectively (ERK and P38 were phosphorylated ERK and phosphorylated P38 ) And cell cycle distribution, and analyze the correlation. The results showed that the mRNA and protein expressions of ERK, P38, cyclin D2 and cyclin E in leukemia cells and K562 cells were increased and the expression of P27 was decreased in CML patients. The expression of cyclin D2 was positively correlated with the expressions of cyclin E, ERK and P38 P <0.01), but negatively correlated with P27 protein expression (P <0.01). G0 / G1 phase cells decreased, S phase cells increased, compared with the control group were significantly different. CONCLUSIONS: The expression and activity of P38 and ERK mRNA are increased in CML, activating the downstream cell cycle regulators of cyclin D2, cyclin E and P27, resulting in the shortening of G0 / G1 phase. The cells rapidly enter the S phase through the G1 / S transition point and accelerate the cell growth Cycle progression and cell proliferation lead to the development of CML.