CAJ | 학술논문

目的　寻求解决维甲酸(ATRA)耐药问题的新途径。方法　光镜、NBT还原实验及免疫荧光间接法观察NB4及其耐药细胞MR-2单用及联用ATRA、γ-干扰素(IFNγ)后细胞形态学、细胞分化及PML蛋白表达的变化。结果　IFNγ单用及与AFRA联用对两种细胞的生长均有抑制作用，IFNγ能诱导PML蛋白的表达，ATRA与IFNγ联用能部分诱导耐药细胞分化结论 IFNγ通过诱导PML蛋白的表达而抑制细胞生长，ATRA与IFNγ联用部分诱导耐药细胞分化的作用可能与两药各自不同的信号传递途径发生交叉激活有关。
목적　심구해결유갑산(ATRA)내약문제적신도경。방법　광경、NBT환원실험급면역형광간접법관찰NB4급기내약세포MR-2단용급련용ATRA、γ-간우소(IFNγ)후세포형태학、세포분화급PML단백표체적변화。결과　IFNγ단용급여AFRA련용대량충세포적생장균유억제작용，IFNγ능유도PML단백적표체，ATRA여IFNγ련용능부분유도내약세포분화 결론 IFNγ통과유도PML단백적표체이억제세포생장，ATRA여IFNγ련용부분유도내약세포분화적작용가능여량약각자불동적신호전체도경발생교차격활유관。
Objective To find new ways to deal with the problem of retinoid resistance. Methods Observation under light microscope, NBT test and indirect fluorescence immunoassay.Results 1. IFNγ alone or combined with ATRA suppresses the growth rate of NB4 as well as MR-2 and high dose IFNγ exerts greater suppression; 2. PML expression is induced by IFNγ; 3. the combination of ATRA and IFNγ partially induces differentiation of the ATRA- resistant promyelocytic cell line.Conclusion IFNγ induces the expression of PML, a growth suppressor and an anti - oncogene, which in consequence suppresses the cell growth. The combined differentiative effect of ATRA and IFNγ on ATRA-resistant cell MR - 2 might be due to the cross talk between the signal pathways of ATRA and IFNs.