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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Differential cell fates induced by all-trans retinoic acid-treated HL-60 human leukemia cells.
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Differential cell fates induced by all-trans retinoic acid-treated HL-60 human leukemia cells.

机译：全反式维甲酸处理的HL-60人白血病细胞诱导的分化细胞命运。

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摘要

HL-60 human leukemia cells, differentiated into a neutrophil lineage by all-trans retinoic acid (ATRA) treatment, express three members of the carcinoembryonic antigen (CEA) gene family, CEA-related cell adhesion molecule 1 (CEACAM1; CD66a), CEACAM3 (CD66d), and CEACAM6 (CD66c). CD66d is a neutrophil lineage-specific marker, and CD66a and CD66c are found on epithelial and other cells. HL-60 cells continuously treated with ATRA underwent apoptosis, and cells transiently treated for 1 day underwent cell-cycle arrest, entered into senescence, and exhibited reduced apoptosis with CD66-positive cells accounting for the majority of live cells. CD66 antigens were also induced in NB4 leukemic cells upon continuous treatment with ATRA. NB4 cells underwent apoptosis with a higher frequency in transient versus continuous-treated cells (38% vs. 19% at Day 5), in contrast to HL-60 cells that underwent cell-cycle arrest and senescence when transiently treated with ATRA. CD66 antigens were not induced in transient, ATRA-treated NB4 cells compared with HL-60 cells. Cell-cycle arrest in HL-60 cells involved reduction in expression levels of p21, cyclins D and E, while Rb1 exhibited reduction in protein levels without changes in mRNA levels over the time course of ATRA treatment. Analysis of several proapoptotic proteins implicated the activation of calpain and cleavage of Bax in the intrinsic apoptotic pathway, similar to published studies about the apoptosis of neutrophils. CD1d expression was also induced by ATRA in HL-60 cells and ligation with anti-CD1d antibody-induced apoptosis. In contrast, CD1d-positive primary monocytes were protected from spontaneous apoptosis by CD1d ligation. These studies demonstrate distinct cell fates for ATRA-treated HL-60 cells that provide new insights into ATRA-induced cell differentiation.
机译：通过全反式维甲酸（ATRA）处理分化为中性粒细胞谱系的HL-60人白血病细胞表达癌胚抗原（CEA）基因家族的三个成员，CEA相关细胞粘附分子1（CEACAM1; CD66a），CEACAM3 （CD66d）和CEACAM6（CD66c）。 CD66d是嗜中性粒细胞谱系特异性标记，在上皮细胞和其他细胞上发现CD66a和CD66c。连续用ATRA处理的HL-60细胞发生凋亡，而经过瞬时处理1天的细胞经历细胞周期停滞，进入衰老状态，并且CD66阳性细胞占大多数活细胞的细胞凋亡减少。在连续用ATRA处理后，NB66白血病细胞中也诱导了CD66抗原。与连续处理的细胞相比，NB4细胞发生凋亡的频率更高（第5天分别为38％和19％），而HL-60细胞则在经过ATRA瞬时处理后经历了细胞周期停滞和衰老。与HL-60细胞相比，在经ATRA处理的瞬时NB4细胞中未诱导CD66抗原。 HL-60细胞的细胞周期停滞涉及p21，细胞周期蛋白D和E的表达水平降低，而Rb1在ATRA治疗期间显示蛋白水平降低而mRNA水平没有变化。几种促凋亡蛋白的分析涉及内在凋亡途径中钙蛋白酶的活化和Bax的裂解，类似于已发表的有关中性粒细胞凋亡的研究。 ATRA还可以在HL-60细胞中诱导CD1d表达，并与抗CD1d抗体诱导的细胞凋亡连接。相反，CD1d阳性的单核细胞通过CD1d的连接被保护免受自发凋亡。这些研究证明了ATRA处理的HL-60细胞具有独特的细胞命运，这为ATRA诱导的细胞分化提供了新的见识。

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