CAJ | 학술논문

目的:探讨recombinanat mutant human TNF-related apoptosis-inducing ligand,(rmhTRAIL)对阿霉素诱导的人慢性粒细胞白血病红白血病变耐药细胞株K562/A02(mdr-1+)的促凋亡作用及其机理.方法:以亲本阿霉素敏感细胞株K562(mdr-1-)为对照,观察rmhTRAIL作用后K562、K562/A02细胞形态变化,采用碘化丙啶染色法流式细胞术(FACSCalibur)定量检测细胞sub-G1%,MTT法测定rmhTRAIL对细胞增殖抑制,半定量逆转录-聚合酶链反应(semiquantitative reverse transcription polymerase chain reaction,RT-PCR)方法检测K562、K562/A02细胞的四种TRAIL受体DcR1、DcR2、DR4、DR5mRNA表达水平.结果:rmhTRAIL可诱导K562、K562/A02细胞凋亡,有典型的细胞形态改变;流式细胞术检测显示K562/A02的sub-G1%大于K562(P＜0.05);rmhTRAIL对K562/A02的增殖抑制作用优于K562(P＜0.05);K562/A02中DR4、DR5mRNA的表达高于K562,DcR1mRNA在K562/A02表达低于K562,DcR2 mRNA在两种细胞中均不表达.结论:rmhTRAIL可以诱导K562/A02细胞凋亡;rmhTRAIL对K562/A02促凋亡和抑制增殖作用优于其亲本细胞K562;K562/A02细胞表面TRAIL死亡受体高表达及诱骗受体低表达可能是耐药细胞更敏感的原因.
목적:탐토recombinanat mutant human TNF-related apoptosis-inducing ligand,(rmhTRAIL)대아매소유도적인만성립세포백혈병홍백혈병변내약세포주K562/A02(mdr-1+)적촉조망작용급기궤리.방법:이친본아매소민감세포주K562(mdr-1-)위대조,관찰rmhTRAIL작용후K562、K562/A02세포형태변화,채용전화병정염색법류식세포술(FACSCalibur)정량검측세포sub-G1%,MTT법측정rmhTRAIL대세포증식억제,반정량역전록-취합매련반응(semiquantitative reverse transcription polymerase chain reaction,RT-PCR)방법검측K562、K562/A02세포적사충TRAIL수체DcR1、DcR2、DR4、DR5mRNA표체수평.결과:rmhTRAIL가유도K562、K562/A02세포조망,유전형적세포형태개변;류식세포술검측현시K562/A02적sub-G1%대우K562(P＜0.05);rmhTRAIL대K562/A02적증식억제작용우우K562(P＜0.05);K562/A02중DR4、DR5mRNA적표체고우K562,DcR1mRNA재K562/A02표체저우K562,DcR2 mRNA재량충세포중균불표체.결론:rmhTRAIL가이유도K562/A02세포조망;rmhTRAIL대K562/A02촉조망화억제증식작용우우기친본세포K562;K562/A02세포표면TRAIL사망수체고표체급유편수체저표체가능시내약세포경민감적원인.