中华血液学杂志
中華血液學雜誌
중화혈액학잡지
Chinese Journal of Hematology
2008年
6期
366-369
,共4页
郑培烝%赵春军%范惠咏%陈玉龙
鄭培烝%趙春軍%範惠詠%陳玉龍
정배증%조춘군%범혜영%진옥룡
分化抑制因子1%全反式维甲酸%白血病,早幼粒细胞,急性%细胞分化
分化抑製因子1%全反式維甲痠%白血病,早幼粒細胞,急性%細胞分化
분화억제인자1%전반식유갑산%백혈병,조유립세포,급성%세포분화
Inhibitor of differentiation 1%All-trans retinoic acid%Acute promyelocytic leukemia%Differentiafion
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.
目的 探討分化抑製因子1(ID1)在全反式維甲痠(ATRA)誘導急性早幼粒細胞白血病(APL)細胞分化中的作用.方法 運用基因芯片、放線菌酮抑製試驗、實時定量RT-PCR和Western blot.方法 檢測ID1存ATRA誘導的APL細胞繫及原代APL細胞分化過程中錶達情況.結果 在ATRA汙導的NB4細胞和APL初診患者原代細胞分化過程巾ID1基因的錶達上調,ATRA誘導NB4細胞2hID1錶達達高峰,其相對錶達水平與對照相比升高359.4±48.7倍;ATRA處理APL患者骨髓細胞ID1錶達水平2 h達高峰,其中1例患者暈複3次檢測的.結果 為對照的(311.1±48.7)倍.而且ID1基因的上調不需要其他蛋白的閤成.而在ATRA處理ATRA耐藥細胞繫NB4-R2細胞未見ID1的錶達髮生明顯變化.結論 ID1基因可能作為ATRA的靶基因參與瞭ATRA誘導的粒繫分化.
목적 탐토분화억제인자1(ID1)재전반식유갑산(ATRA)유도급성조유립세포백혈병(APL)세포분화중적작용.방법 운용기인심편、방선균동억제시험、실시정량RT-PCR화Western blot.방법 검측ID1존ATRA유도적APL세포계급원대APL세포분화과정중표체정황.결과 재ATRA오도적NB4세포화APL초진환자원대세포분화과정건ID1기인적표체상조,ATRA유도NB4세포2hID1표체체고봉,기상대표체수평여대조상비승고359.4±48.7배;ATRA처리APL환자골수세포ID1표체수평2 h체고봉,기중1례환자훈복3차검측적.결과 위대조적(311.1±48.7)배.이차ID1기인적상조불수요기타단백적합성.이재ATRA처리ATRA내약세포계NB4-R2세포미견ID1적표체발생명현변화.결론 ID1기인가능작위ATRA적파기인삼여료ATRA유도적립계분화.
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.