全反式维甲酸诱导急性早幼粒细胞白血病细胞分化中分化抑制因子1表达水平的变化

目的 探讨分化抑制因子1(ID1)在全反式维甲酸(ATRA)诱导急性早幼粒细胞白血病(APL)细胞分化中的作用.方法 运用基因芯片、放线菌酮抑制试验、实时定量RT-PCR和Western blot.方法 检测ID1存ATRA诱导的APL细胞系及原代APL细胞分化过程中表达情况.结果 在ATRA污导的NB4细胞和APL初诊患者原代细胞分化过程巾ID1基因的表达上调,ATRA诱导NB4细胞2hID1表达达高峰,其相对表达水平与对照相比升高359.4±48.7倍;ATRA处理APL患者骨髓细胞ID1表达水平2 h达高峰,其中1例患者晕复3次检测的.结果 为对照的(311.1±48.7)倍.而且ID1基因的上调不需要其他蛋白的合成.而在ATRA处理ATRA耐药细胞系NB4-R2细胞未见ID1的表达发生明显变化.结论 ID1基因可能作为ATRA的靶基因参与了ATRA诱导的粒系分化.

Expression level changes of inhibitor of differentiation 1 during ATRA-induced acute promyelocytic leukemia cells differentiation

Objective To study the role of inhibitor of differentiation l(Idl)in ATRA-induced a-cute promyelocytic leukemia(APL)cells differentiation.Methods The expression of Idl was detected by cDNA microarray.Cycloheximide inhibition test.Real-time RT-PCR and western blot.Results The expres-sion of Idl gene was up-regulated in ATRA-induced NB4 cells and APL cells from two patients and was inde-pendent on other proteins synthesis.Idl expression level reached the peak at 2 h in NB4 cells induced by ATRA.Its relative expression level was(359.4±48.7)-fold greater than contro1.Idl expression level reached the peak at 2 h in bone marrow cells from APL patents treated with ATRA.And itS level detected 3 times in one of the patient was(311.1±48.7)fold of contro1.The expression of Idl protein was not up-reg-ulated in ATRA resistant NB4-R2 cells after ATRA treatment.Conclusion Idl may be involved in ATRA-induced granulocytic difierentiation as an ATRA-targeted gene.