Regulation of desaturase expression in HL60 cells

The expression of delta 5 desaturase (D5D), delta 6 desaturase (D6D) and delta 9 desaturase (D9D) was determined by RT‐PCR in the human promyelocytic cell line HL60. During 72?h of culture with 10?% FBS, D5D and D6D were upregulated 5 to 6‐fold, whereas D9D approximately doubled. The addition of fatty acids (FAs) to the culture medium suppressed upregulation of all desaturases. N‐3 and n‐6 FA appeared to be more effective than n‐9 or saturated FA. When FAs were added after 72?h, further upregulation during the next 24?h was suppressed for nearly all desaturases and FAs tested, except for D5D when oleic acid (OA) or stearic acid (SA) was added. In cells cultured with restricted amounts of FBS, desaturase expression increased with decreasing concentrations of FBS. Cellular FA content decreased by 60?% in the neutral lipid fraction, whereas that of the phospholipid fraction decreased by 10?% during 72?h of culture. The largest decrease occurred in the sum of n‐3 and n‐6 FA of the neutral lipid fraction, which was reduced by 83?%, whereas the content of these FAs in the phospholipid fraction decreased by 32?%. The results indicate that when the supply of FA to HL60 cells is limited, the intracellular content of n‐3 and n‐6 FA decreases and this leads to upregulation of the desaturases, particularly D5D and D6D. Since HL60 cells resemble human leukocytes, the results suggest that desaturase expression in leukocytes may be exploited as a biomarker for FA status.     

柴胡皂甙d上调HL-60细胞糖皮质激素受体mRNA并诱导细胞凋亡

目的　观察柴胡皂甙d(SSd)对HL 6 0细胞糖皮质激素受体 (GR)mRNA表达的调节作用以及对细胞凋亡的影响。方法　选用从柴胡中提取的单体成分SSd ,以3 H 胸腺嘧啶掺入法观察SSd对细胞生长的抑制作用 ,DNA凝胶电泳及流式细胞术分析细胞凋亡 ,用Northernblot分析GRmRNA的改变。结果　经SSd作用后 ,HL 6 0细胞3 H 胸腺嘧啶掺入率明显降低 ,呈时间和剂量依赖关系 ,10 μg/mlSSd处理 48小时作用最明显 ,6 0小时时出现典型的DNA片段梯形带 ,流式细胞仪分析细胞阻滞于G1期并出现凋亡峰 ;GRmRNA表达增加。结论　SSd可上调HL 6 0细胞GRmRNA表达并诱导细胞凋亡。     

9—顺式维甲酸诱导HL—60细胞凋亡

目的：检测９－顺式维甲酸（９－ｃｉｓＲＡ）诱导ＨＬ－６０细胞凋亡的能力，并探讨其分子机制。方法：应用形态学观察、ＤＮＡ电泳、流式细胞仪分析检测细胞凋亡，应用流式细胞仪检测ＨＬ－６０细胞ｂｃｌ－２含量。结果：９－ｃｉｓＲＡ可以诱导ＨＬ－６０细胞在分化后发生典型的凋亡。在ＨＬ－６０细胞分化和凋亡的过程中ｂｃｌ－２含量逐渐下降。９－ｃｉｓＲＡ诱导ＨＬ－６０细胞凋亡能力和降低ｂｃｌ－２表达的能力均显著强于全反式维甲酸（Ａ－ＴＲＡ）。结论：９－ｃｉｓＲＡ具有诱导ＨＬ－６０细胞凋亡的作用。ｂｃｌ－２表达水平的降低可能是经诱导分化成熟的白血病细胞走向凋亡的重要条件。     

Differentiation-stimulating potency of differentiated HL60 cells after drug treatment

Differentiation therapy in the treatment of leukemia is often hampered by limitations on using certain pharmaceutical regents or on the required doses due to various reasons, such as drug-resistance and retinoic acid syndrome. To circumvent these problems, a strategy might be developed on the basis of the ability of drug-differentiated cells to stimulate differentiation in leukemia cells. Using the promyelocytic leukemia cell line HL60 as a cell model, we assessed the differentiation-stimulating potency of differentiated granulocytes and monocytes/macrophages after treatments with all-trans retinoic acid (ATRA) and 12-O-tetradecanoylphorbol-13-acetate (TPA), respectively. ATRA- and TPA-differentiated cells were able to stimulate differentiation in fresh HL60 cells, accompanied by inhibition on cell growth to various extents. The differentiated cells of the second generation, especially those originated from TPA treatment, were as potent as the drugs themselves in stimulating differentiation in fresh HL60 cells. On the basis of “differentiation induced by differentiated cells”, we explored the feasibility of ex vivo therapy.     

Characterization of transferrin receptor-dependent GaC-Tf-FeN transport in human leukemic HL60 cells

BACKGROUND: Understanding the uptake of GaC-Tf-FeN by cells will provide key insights into studies on transferrin-mediated drug delivery. METHODS: The mechanism of GaC-Tf-FeN transporting into and out of HL60 cells has been investigated by comparing transports between GaC-Tf-FeN and apoTf by means of 125I-labeled transferrin. RESULTS: An association constant for GaC-Tf-FeN was 2 times that for apoTf. GaC-Tf-FeN and apoTf of cell surface-bound displayed similar kinetics during the uptake, but the release rates of internalized GaC-Tf-FeN and apoTf from cells were different which showed characteristic disparate. The release continued to occur during the incubation of GaC-Tf-FeN in the presence of nonradioactive apoTf. Neither NaN3 nor NH4Cl could completely block internalization of GaC-Tf-FeN, but they prevented the release of GaC-Tf-FeN from the cells. Excess cold unlabeled apoTf could overcome the block in the release due to NH4Cl but not NaN3. The binding and internalization of GaC-Tf-FeN could be competitively inhibited by nonradioactive apoTf. It implies that both bind to the same receptor on the membrane and the localization of GaC-Tf-FeN resembles that of apoTf inside cells. Pretreated cells with pronase abolished the binding of GaC-Tf-FeN significantly. CONCLUSION: On the basis of these findings, we proposed the "transferrin receptor" for the mechanism of GaC-Tf-FeN transport by HL60 cells.     

Inhibition of c-fes expression by an antisense oligomer causes apoptosis of HL60 cells induced to granulocytic differentiation

The c-fes protooncogene is expressed at high levels in the terminal stages of granulocytic differentiation, but so far no definite function has been attributed to the product of this oncogene. To tackle this problem, the c-fes protooncogene expression has been inhibited in HL60 cells, and fresh leukemic promyelocytes of acute promyelocytic leukemia have been induced to differentiate with retinoic acid (RA) and dimethylsulfoxide (DMSO). Inhibition was obtained by incubating the cells with a specific c-fes antisense oligodeoxynucleotide. It was observed that the cells, rather than differentiating, underwent premature cell death showing the morphological and molecular characteristics of apoptosis. This process was inhibited by granulocyte and granulocyte/macrophage colony-stimulating factor, but not by interleukin 3 (IL-3), IL-6, or stem cell factor. Our present results demonstrate that the loss of cell viability that occurs during the in vitro differentiation of myeloid cells, after the complete inhibition of the c-fes gene product and treatment with RA-DMSO, is due to activation of programmed cell death. It is concluded that a possible role of the c-fes gene product is to exert an antiapoptotic effect during granulocytic differentiation.     

三氧化二砷逆转HL60/ADR细胞耐药的研究

背景:临床应用三氧化二砷(As2O3)治疗复发难治性急性早幼粒细胞白血病已获得较好效果。目的:探讨As2O3逆转急性髓系白血病细胞株HL60/ADR耐药的作用及其机制。方法:以HL60/ADR细胞为研究对象,分为空白对照组和As2O3组,空白对照组不加任何药物培养,As2O3组加入48hIC50As2O3进行培养。结果与结论:As2O3能提高HL60/ADR细胞摄取阿霉素水平,降低HL60/ADR细胞多药耐药相关蛋白1表达率(P<0.05),能够促进HL60/ADR细胞凋亡,细胞早期和晚期凋亡率均高于空白对照组(P<0.01),并随时间增加而提高。可减低细胞IκBα、p65、抗凋亡蛋白Bcl-2表达,使促凋亡蛋白Bax,断裂的Caspase-3、Caspase-9、PARP表达升高,说明As2O3能够逆转HL60/ADR细胞耐药,与其上述变化有关。     

三氧化二砷逆转HL60/ADR细胞耐药的研究

背景：临床应用三氧化二砷（As2O3）治疗复发难治性急性早幼粒细胞白血病已获得较好效果。目的：探讨As2O3逆转急性髓系白血病细胞株HL60/ADR耐药的作用及其机制。方法：以HL60/ADR细胞为研究对象,分为空白对照组和As2O3组,空白对照组不加任何药物培养,As2O3组加入48hIC50As2O3进行培养。结果与结论：As2O3能提高HL60/ADR细胞摄取阿霉素水平,降低HL60/ADR细胞多药耐药相关蛋白1表达率（P〈0.05）,能够促进HL60/ADR细胞凋亡,细胞早期和晚期凋亡率均高于空白对照组（P〈0.01）,并随时间增加而提高。可减低细胞IκBα、p65、抗凋亡蛋白Bcl-2表达,使促凋亡蛋白Bax,断裂的Caspase-3、Caspase-9、PARP表达升高,说明As2O3能够逆转HL60/ADR细胞耐药,与其上述变化有关。     

硫酸软骨素对HL60细胞增殖分化的影响

背景:硫酸软骨素是细胞基质的重要成分,可促进肿瘤细胞的增殖,抑制其转移。目的:观察硫酸软骨素对阿霉素作用下HL60细胞增殖分化的影响。设计:开放性实验。单位:青岛大学医学院生物化学与分子生物学教研室。材料:实验于2003-09/2004-12在青岛大学医学院生物化学与分子生物学研究室完成。HL60细胞株购于中国医学科学院上海细胞库,为人类早幼粒白血病细胞。牛软骨硫酸软骨素(Sigma)。方法:①细胞传代培养后将进入对数增殖期的细胞用含体积分数0.1灭活胎牛血清的RPMI1640培养液配制成1×108L-1的细胞悬液,分装于45个培养瓶中,4mL/瓶。②取分装好的细胞悬液15瓶,按照0,5,25,50,75mg/L浓度加入硫酸软骨素,每个浓度平行3瓶,空白对照组加入等量的0.01mol/L磷酸盐缓冲液。采取细胞计数法测定硫酸软骨素处理后的HL60细胞密度的变化。③取分装好的细胞悬液30瓶,分为硫酸软骨素 阿霉素组、硫酸软骨素组,各15瓶。按照0,5,25,50,75mg/L浓度向两组加入硫酸软骨素,每个浓度平行3瓶,空白对照组加入等量的0.01mmol/L磷酸盐缓冲液。用MTT法测定硫酸软骨素处理后的HL60细胞加入阿霉素后细胞存活率的变化。④取分装好的细胞悬液15瓶,按照0,5,25,50,75mg/L浓度加入硫酸软骨素,每个浓度平行3瓶,空白对照组加入等量的0.01mol/L磷酸盐缓冲液。用酶联免疫反应测定各组细胞的酸性磷酸酶活性,观察其对细胞分化的影响。主要观察指标:①硫酸软骨素对HL60细胞增殖的影响。②硫酸软骨素 阿霉素对HL60细胞存活率的影响。③硫酸软骨素对HL60细胞酸性磷酸酶活性的影响。结果:共制备细胞悬液45瓶,全部进入结果分析。①与空白对照组比较,不同浓度硫酸软骨素处理24h后HL60细胞密度均显著升高(P<0.01);且50,75mg/L硫酸软骨素浓度组的细胞密度升高尤为明显,但两组间比较基本相似(P>0.05),说明在这个浓度范围内硫酸软骨素对细胞生长的促进作用变化不大。②与空白对照组比较,加入不同浓度硫酸软骨素后,硫酸软骨素 阿霉素组细胞存活率均有不同程度的降低,硫酸软骨素浓度超过25mg/L时降低明显(P<0.01)。③与空白对照组比较,5,25,50mg/L硫酸软骨素浓度组HL60细胞酸性磷酸酶吸光度值均明显升高(1.268±0.038,1.305±0.101,1.321±0.021,1.354±0.013,P<0.01或0.05),尤其是75mg/L硫酸软骨素浓度组HL60细胞酸性磷酸酶吸光度值高达1.406±0.113,与空白对照组比较差异有极显著意义(P<0.001)。结论:硫酸软骨素在适当浓度时对HL60细胞的增殖产生促进作用,可提高HL60细胞对阿霉素的敏感性,促进细胞分化。     

硫酸软骨素对HL60细胞增殖分化的影响

背景：硫酸软骨素是细胞基质的重要成分，可促进肿瘤细胞的增殖，抑制其转移。 目的：观察硫酸软骨素对阿霉素作用下HL60细胞增殖分化的影响。 设计：开放性实验。 单位：青岛大学医学院生物化学与分子生物学教研室。 材料：实验于2003—09／2004—12在青岛大学医学院生物化学与分子生物学研究室完成。HL60细胞株购于中国医学科学院上海细胞库，为人类早幼粒白血病细胞。牛软骨硫酸软骨素（Sigma）。 方法：①细胞传代培养后将进入对数增殖期的细胞用含体积分数0．1灭活胎牛血清的RPMI1640培养液配制成1&;#215;10^8L^-1的细胞悬液，分装于45个培养瓶中，4mL／瓶。②取分装好的细胞悬液15瓶，按照0，5，25，50，75肿g／L浓度加入硫酸软骨素，每个浓度平行3瓶，空白对照组加入等量的0．01mol／L磷酸盐缓冲液。采取细胞计数法测定硫酸软骨素处理后的HL60细胞密度的变化。③取分装好的细胞悬液30瓶，分为硫酸软骨素＋阿霉素组、硫酸软骨素组，各15瓶。按照0，5，25，50，75mg／L浓度向两组加入硫酸软骨素，每个浓度平行3瓶，空白对照组加入等量的0．01mmol／L磷酸盐缓冲液。用MTT法测定硫酸软骨素处理后的HL60细胞加入阿霉素后细胞存活率的变化。④取分装好的细胞悬液15瓶，按照0，5，25，50，75mg／L浓度加入硫酸软骨素，每个浓度平行3瓶，空白对照组加入等量的0.01mol／L磷酸盐缓冲液。用酶联免疫反应测定各组细胞的酸性磷酸酶活性，观察其对细胞分化的影响。 主要观察指标：①硫酸软骨素对HL60细胞增殖的影响。②硫酸软骨素＋阿霉素对HL60细胞存活率的影响。③硫酸软骨素对HL60细胞酸性磷酸酶活性的影响。 结果：共制备细胞悬液45瓶，全部进入结果分析。①与空白对照组比较，不同浓度硫酸软骨素处理24h后HL60细胞密度均显著升高（P〈0．01）；且50，75mg／L硫酸软骨素浓度组的细胞密度升高尤为明显，但两组间比较基本相似（P〉0．05），说明在这个浓度范围内硫酸软骨素对细胞生长的促进作用变化不大。②与空白对照组比较，加入不同浓度硫酸软骨素后，硫酸软骨素＋阿霉素组细胞存活率均有不同程度的降低，硫酸软骨素浓度超过25mg／L时降低明显（P〈0．01）。③与空白对照组比较，5，25，50mg／L硫酸软骨素浓度组HL60细胞酸性磷酸酶吸光度值均明显升高（1．268&;#177;0．038，1．305&;#177;0．101，1．321&;#177;0.021．1．354&;#177;0．013，P〈0．01或0.05），尤其是75mg／L硫酸软骨素浓度组HL60细胞酸性磷酸酶吸光度值高达1．406&;#177;0．113，与空白对照组比较差异有极显著意义（P〈0．001）。 结论：硫酸软骨素在适当浓度时对HL60细胞的增殖产生促进作用，可提高HUD细胞对阿霉素的敏感性，促进细胞分化。     

足叶乙甙诱导HL-60细胞凋亡过程中电化学行为的研究

目的研究药物诱导白血病细胞凋亡中的电化学变化及其意义。方法使用电化学传感器检测经足叶乙甙（Ｖｐ１６）诱导的ＨＬ６０细胞凋亡。结果２～２００μｇ／ｍｌＶｐ１６作用于ＨＬ６０细胞２４小时的过程中,随着药物剂量的增大,细胞峰值电流逐渐降低,Ｖｐ１６２μｇ／ｍｌ时即可观察到细胞电化学活性较对照组下降,２０μｇ／ｍｌ时明显下降。以Ｖｐ１６２００μｇ／ｍｌ诱导细胞凋亡,通过ＤＮＡ含量分析显示在２,３,４小时细胞凋亡率为１０．５％～２０．０％,用电化学传感器方法检测细胞电化学活性改变差异明显,峰值电流从１．８μＡ降至０４μＡ,４小时时峰值电流降至用药前的１／５。结论在细胞凋亡早期启动阶段的电化学信号改变具有一定的早期意义和蓄积性。     

2-甲氧雌二醇对HL60白血病细胞增殖和凋亡的影响

目的探讨2-甲氧雌二醇对HL60白血病细胞增殖及凋亡的影响。方法运用四唑蓝（MTT）法和彗星电泳法检测2-甲氧雌二醇对HL60白血病细胞的增殖抑制及促凋亡作用;应用流式细胞技术检测Bcl-2蛋白的表达。结果（1）2-甲氧雌二醇在10～50μM浓度范围内作用72h以及30μM2-甲氧雌二醇在作用24、48、72h后对HL60白血病细胞有增殖抑制作用,这种作用呈时间-剂量依赖关系。（2）2-甲氧雌二醇在作用浓度为10、30、50μM时,HL60白血病细胞凋亡率分别为8．20％、28．20％、45．30％,与阴性对照组（1．00％）差异有统计学意义;30μM2-甲氧雌二醇在作用24、48、72h后,HL60白血病细胞凋亡率分别为3．71％、17．72％、43．58％,48、72h作用时间组与阴性对照组（1．00％）差异有统计学意义。（3）30μM2-甲氧雌二醇作用72h后的细胞,Bcl-2蛋白的表达较对照组显著减少。结论2-甲氧雌二醇具有对HL60白血病细胞增殖抑制及促凋亡作用,Bcl-2蛋白表达下调在此过程中可能发挥着重要的作用。     

ICAT干扰慢病毒表达载体构建及稳转HL60细胞株的建立

目的构建ICAT基因的干扰慢病毒表达载体,建立稳定转染的HL60细胞系。方法人工设计、合成针对ICAT基因干扰序列,退火后连接到PGLV3干扰载体上,与PG-p1-VSVG、PG-p1-REV、PG-p1-RRE共转染293T细胞,包装产生慢病毒颗粒并测定病毒滴度,感染HL60细胞,建立稳定细胞株;应用RT-PCR和Western Blot技术检测HL60稳定细胞中ICAT基因和蛋白表达情况,并与对照组进行比较。结果成功构建了针对ICAT基因的RNAi慢病毒表达载体,病毒滴度为2×10~8 TU/mL;建立稳定转染的HL60细胞株。有效干扰验证显示,shICAT能明显降低ICAT的mRNA及蛋白水平(P0.001)。结论成功构建ICAT基因的shRNA慢病毒表达载体,建立稳定干扰ICAT表达的HL60细胞株。     

hKSR-2, a vitamin D-regulated gene, inhibits apoptosis in arabinocytosine-treated HL60 leukemia cells

Ras signaling can be modulated by the scaffolding activity of kinase suppressor of Ras-1 (KSR-1) and by the hKSR-2 protein, resulting in diverse phenotypic outcomes. The mitogen-activated protein kinase cascade downstream from Ras and KSRs includes Raf-1 and extracellular signal-regulated kinase 1/2 kinases, known to enhance survival potential of a range of cell types. Because the molecular events that increase survival of HL60 cells induced to differentiate toward monocytic phenotype by 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] are not known, we investigated if KSR proteins provide a survival function in these cells. We found that whereas kinase suppressor of Ras-1 had no detectable effect on cell survival in the system studied here, 1,25-(OH)2D3-induced up-regulation of hKSR-2 enhanced the resistance of HL60 cells to arabinocytosine. Knockdown of hKSR-2 by either small interfering RNA or antisense oligonucleotides increased arabinocytosine-induced apoptosis, which was accompanied by reduced Bcl-2/Bax and Bcl-2/Bad ratios, and increased caspase-3 activating cleavage. In contrast, up-regulation of Mcl-1 was not abrogated by anti-sense (AS) AS-hKSR-2, pointing to a specific role of Bcl-2 in control of 1,25-(OH)2D3-induced increased cell survival. These findings are consistent with the previously shown lack of fully differentiated monocytic cells in HL60 cultures exposed to 1,25-(OH)2D3 in which hKSR-2 was knocked down, suggesting that optimal differentiation of these cells requires enhanced antiapoptotic mechanisms provided, at least in part, by hKSR-2. Collectively, these results suggest that hKSR-2 may offer a new target for novel therapies of acute myelogenous leukemia.     

黄酮联合阿霉素协同诱导HL60/ADR细胞凋亡机制的研究

目的:探究黄酮在体外对多药耐药细胞系HL60/ADR的影响及联合阿霉素后对细胞生长抑制和凋亡的作用机制,探讨中药在白血病化疗中扶正、增效的可能性。方法:用CCK-8法检测黄酮和阿霉素对HL60/ADR细胞生长的抑制作用;用流式细胞仪检测药物作用后的细胞凋亡率,并在光镜下观察细胞形态变化;蛋白印迹法检测药物作用后凋亡信号通路蛋白表达的情况;流式细胞仪检测药物作用后HL60/ADR线粒体跨膜电位的变化。结果:黄酮能显著抑制HL60/ADR细胞的增殖,且其抑制细胞增殖效应呈现浓度-时间依赖性;不同浓度的黄酮及联合阿霉素1.5μg/mL(20%抑制浓度即IC20值)后对细胞的抑制作用更明显,具有协同和相加作用。75μg/mL和100μg/mL黄酮能促进HL60/ADR细胞凋亡,而黄酮联合阿霉素的促凋亡作用更显著。蛋白信号通路研究显示,单药黄酮及两药联合能使HL60/ADR细胞线粒体膜电位下降,抗凋亡蛋白Bcl-2、Bcl-XL表达明显下调,促凋亡蛋白Bim、Bad、Bax明显增加,激活caspase途径;同时磷酸化的P-JNK蛋白表达水平升高,而P-ERK明显下降。结论:黄酮联合阿霉素可通过线粒体跨膜电位的下降,依赖caspase活化调控Bcl-2家族中Bim、Bad和Bax蛋白表达,下调ERK细胞保护通路并上调JNK应激相关通路,最终协同抑制HL60/ADR细胞增殖并诱导其凋亡。     

IQF characterization of a cathepsin B-responsive nanoprobe for report of differentiation of HL60 cells into macrophages

Tracking of in vivo fates of exogenous cell transplants in terms of viability, migration, directional differentiation and function delivery by a suitable method of medical imaging is of great significance in the development and application of various cell therapies. In this contribution directional differentiation of HL60 cells into macrophages and granulocytes, and a difference in the associated expression level of cathepsin B (Cat B) among the parent and daughter cells is used as a model to guide and evaluate the development of a Cat B-responsive Abz-FRFK-Dnp@PLGA nanoprobe for an optical report of the differentiation process. A well-documented internally quenched fluorescence (IQF) pair coupled with a peptide substrate FRFK of Cat B was synthesized and imbedded in PLGA to form the nanoprobe. The nanoprobe is resistant to leakage when dispersed in water for 10 days. Degradation of the nanoprobe is dominated by Cat B. HL60 cells were then labelled with the Abz-FRFK-Dnp@PLGA nanoprobe to track the differentiation process. Differentiation of labelled HL60 cells into macrophages exhibited a significantly higher fluorescence relative to the granulocytes or the labelled parent cells. The fluorescence difference allows the differentiation process to be followed. The established characterization and assessment procedure is to be used for the development and evaluation of nanoprobes for other imaging modalities.

A Cat B-responsive Abz-FRFK-Dnp@PLGA nanoprobe for an optical report of the differentiation of HL60 cells into macrophages.     

维甲酸诱导HL-60细胞Fas蛋白表达

目的：探讨全反式维甲酸（ＡＴＲＡ）和９顺式维甲酸（９ｃｉｓＲＡ）对ＨＬ６０细胞Ｆａｓ表达水平及维甲酸对抗Ｆａｓ抗体诱导的细胞凋亡敏感性的影响。方法：用流式细胞仪检测ＨＬ６０细胞膜Ｆａｓ蛋白表达水平；分别采用形态学观察、ＤＮＡ电泳和流式细胞仪检测抗Ｆａｓ抗体诱导的细胞凋亡。结果：ＨＬ６０细胞Ｆａｓ弱表达。经１０－６ｍｏｌ／ＬＡＴＲＡ或９ｃｉｓＲＡ分别预处理４天后，ＨＬ６０细胞Ｆａｓ表达水平及对抗Ｆａｓ抗体诱导凋亡的敏感性均显著提高。９ｃｉｓＲＡ提高ＨＬ６０细胞对抗Ｆａｓ抗体诱导凋亡的敏感性的能力强于ＡＴＲＡ。结论：维甲酸可上调ＨＬ６０细胞表达Ｆａｓ，这可能与维甲酸诱导ＨＬ６０细胞分化相关。进一步深入探讨其分子机制，将为肿瘤治疗，特别是自体骨髓移植中骨髓净化提供新方法     

六亚甲基二乙酰胺对HL60细胞分化和凋亡的影响

目的：研究六亚甲基二乙酰胺（HMHA）诱导HL60细胞分化和凋亡的作用。方法：流式细胞仪（FcM）检测HL60细胞分化抗原CD11b、CD14和CD68抗原表迭，Annexin V／H染色法测定HMBA时HL60细胞凋亡的作用，FCM检测HMBA对于HL60细胞细胞周期的影响。结果：HMBA作用72h后，HL60细胞CD11b抗原表达明显上调，表明HMBA诱导HL60细胞向成熟粒系分化；同时HMBA具有很弱的诱导HL60细胞凋亡的作用；HMBA作用后HL60细胞被阻滞于细胞周期的G0／G1期。结论：HMBA对HL60细胞的作用主要是促进分化，诱导凋亡不是主要作用机制；HMBA阻滞HL60细胞于G0／G1期，这种细胞周期阻滞作用可能是HMBA促分化作用的基础。