Selective induction of apoptosis by ar-turmerone isolated from turmeric (Curcuma longa L) in two human leukemia cell lines, but not in human stomach cancer cell line

We have investigated the effects of ar-turmerone isolated from turmeric (Curcuma longa L) on DNA of human leukemia cell lines, Molt 4B, HL-60 and stomach cancer KATO III cells. It was found that selective induction of apoptosis by ar-turmerone was observed in human leukemia Molt 4B and HL-60 cells, but not in human stomach cancer KATO III cells. Morphological changes showing apoptotic bodies were observed in the human HL-60 and Molt 4B cells treated with ar-turmerone. The fragmentation of DNA by ar-turmerone to oligonucleosomal-sized fragments that is a characteristic of apoptosis was observed to be concentration- and time-dependent in Molt 4B and HL-60 cells, but not in KATO III cells. The data of the present study show that the suppression by ar-turmerone of growth of these leukemia cell lines results from the induction of apoptosis by this compound.     

Glycyrrhizin induces apoptosis in human stomach cancer KATO III and human promyelotic leukemia HL-60 cells

We have investigated the effects of glycyrrhizin (GL) on cell proliferations of human stomach cancer KATO III and promyelotic leukemia HL-60 cells, and on DNA of those cell lines. GL displayed growth inhibitory effect against KATO III and HL-60 cells. Morphological change showing apoptotic bodies was observed in the KATO III and HL-60 cells treated with GL. The fragmentation of DNA by GL to oligonucleosomal-sized fragments that is a characteristic of apoptosis was observed to be concentration- and time-dependent in both cell lines. Caspase inhibitors such as Z-VAD-FMK and Z-Asp-CH2-DCB suppressed the DNA fragmentation induced by GL. The data of the present study show that the suppression of KATO III and HL-60 cell-growth by GL results from the induction of apoptosis by GL, and that caspase is involved in the induction of apoptosis by GL in these cells.     

Glycyrrhetic acid (a metabolic substance and aglycon of glycyrrhizin) induces apoptosis in human hepatoma, promyelotic leukemia and stomach cancer cells

We have investigated the effect of glycyrrhetic acid (GR) which is metabolic substance of glycyrrhizin, on DNA of human hepatoma (HLE), promyelotic leukemia (HL-60) and stomach cancer (KATO III) cells. GR displayed apoptotic effects against HLE, HL-60 and KATO III cells. The fragmentation of DNA by GR to oligonucleosomal-sized fragments, a characteristic of apoptosis, was dose- and time-dependent in these cell lines. These findings suggest that growth inhibition of these cell lines by GR result from the induction of apoptosis by the compound. Inhibitors of caspases did not suppress the DNA fragmentation caused by GR. N-acetyl-L-cysteine, an antioxidant drug, weakly inhibited the DNA fragmentation caused by GR suggesting that active oxidants work partly as an apoptosis-inducing transfer substance.     

2-O-methylisohemigossylic acid lactone, a sesquiterpene, isolated from roots of mokumen (Gossampinus malabarica) induces cell death and morphological change indicative of apoptotic chromatin condensation in human promyelotic leukemia HL-60 cells

2-O-methylisohemigossylic acid lactone, a sesquiterpene, was purified from roots of mokumen (Gossampinus malabarica) and identified by Mass, and (1)H- and (13)-NMR. This sesquiterpene displayed strong growth inhibitory effect against human promyelotic leukemia HL-60 cells. Apoptotic morphological change of the nucleus, including chromatin condensation was induced in the HL-60 cells treated with the sesquiterpene. The fragmentation of DNA by the sesquiterpene to oligonucleosomal-sized fragments, a characteristic of apoptosis, was observed to be dose- and time-dependent in the HL-60 cells. Inhibitors of caspases suppressed the DNA fragmentation induced by the sesquiterpene. These findings suggest that growth inhibition by the sesquiterpene of HL-60 cells results from the induction of apoptosis by the sesqui-terpene, and that caspase cascade is involved in the induction of apoptosis by the compound in the HL-60 cells.     

Induction of apoptosis by three types of procyanidin isolated from apple (Rosaceae Malus pumila) in human stomach cancer KATO III cells

We have investigated the effects of three types of procyanidin isolated from apple (Rosaceae Malus pumila) on DNA of human stomach cancer KATO III cells. Induction of apoptosis by these procyanidins was observed in human stomach cancer KATO III cells. Morphological changes showing apoptotic bodies were observed in the KATO III cells treated with procyanidins. The fragmentation of DNA by procyanidins to oligonucleosomal-sized fragments, a characteristic of apoptosis, was observed to be concentration- and time-dependent in the KATO III cells. N-acetyl-L-cysteine, an antioxidant, suppressed the DNA fragmentation induced by these procyanidins. The present study shows that the suppression of KATO III cell-growth by three types of procyanidin results from the induction of apoptosis by these compounds, and that active oxygen is involved in the induction of apoptosis by these compounds in the KATO III cells.     

茶多酚对HL-60细胞株体外增殖及细胞周期的影响

目的 探讨茶多酚对人急性早幼粒白血病细胞株HL-60细胞增殖和细胞周期的影响.方法 采用四甲基偶氮唑盐微量酶反应比色法(MTT比色法)观察茶多酚对体外培养的HL-60细胞增殖活性的影响.采用HE染色、荧光染色观察用茶多酚后细胞形态变化.用流式细胞仪(FACS)检测细胞凋亡率及细胞周期.结果 (1)MTT比色法检测显示茶多酚能抑制HL-60细胞增殖,在一定范围内呈剂量和时间依赖性(P＜0.05).当茶多酚浓度达到400和800 mg/L时,48 h抑制率分别为(58.90±1.19)%和(72.57±0.70)%.(2)流式细胞仪分析,茶多酚处理组出现一特征性的亚二倍体凋亡峰.其凋亡率呈时间、剂量依赖性.(3)流式细胞术发现茶多酚可使HL-60细胞阻滞于S期,其阻滞细胞的数量与药物浓度呈正相剂量关系,以作用24 h对细胞周期的阻滞作用最强.结论 茶多酚能有效抑制HL-60细胞增殖,在一定范围内具有时间和剂量依赖性.茶多酚可体外诱导HL-60细胞凋亡,并使细胞周期阻滞于S期.     

SU11248对白血病细胞HL-60增殖及凋亡作用的实验研究

目的:探讨新型抗肿瘤药物苹果酸舒尼替尼(SU11248)对白血病细胞HL-60的生物学效应的影响及其作用机制。方法:应用MTT法检测SU11248对HL-60细胞增殖能力的影响;用AnnexinV/PI双染流式细胞术检测细胞凋亡;用流式细胞技术分析细胞的DNA倍体及细胞周期变化;用凝胶电泳分析DNA片段化;以Western blot法检测2.0μg/ml SU11248作用HL-60后bcl-2、bax、caspase-3蛋白水平的变化。结果:SU11248可明显抑制HL-60细胞增殖(P<0.05),呈剂量和时间依赖性,半数抑制浓度(IC50)约为2.00μg/ml。SU11248可促进细胞凋亡,并呈剂量依赖性;能将HL-60细胞阻滞于G0/G1期,并呈时间依赖性;诱导HL-60细胞呈典型的DNA梯带;SU11248作用后bcl-2蛋白表达随时间依赖性降低,caspase-3蛋白表达升高,bax蛋白表达无明显变化。结论:SU11248能抑制HL-60细胞增殖,诱导其凋亡,调节bcl-2家族蛋白的表达,并裂解caspase-3是其可能作用机制之一。     

Vitamin K2-induced antitumor effects via cell-cycle arrest and apoptosis in gastric cancer cell lines

Vitamin K2 (VK2) has a growth inhibitory effect on various types of cancer cells in vitro, and its efficacy has been demonstrated in clinical applications in a number of patients with leukemia and hepatocellular carcinoma. In this study, the effect of cell growth inhibition and apoptosis induction and the concomitant use of an anticancer agent by VK2 (menaquinone: MK4), on gastric cancer cell lines were examined. When 4 kinds of gastric cancer cells (KATO III, MKN7, MKN74 and FU97) were exposed to MK4, the cell growth was inhibited in an MK4 dose-dependent manner. Morphologically, apoptosis induced by MK4 was recognized in FU97, but only a slight number of apoptotic images was recognized in other cell lines. On the contrary, in all the cell lines, the percentage of APO2.7 positive cells increased significantly in the MK4-treated group as compared to the controls. Caspase-3 activity increased significantly in KATO III and FU97 as compared to the controls, while no significant differences were noted in MKN7 or MKN74. Moreover, in all the cell lines, the percentage of G0/G1-phase cells ( approximately 70% in KATO III and FU97, and > or =80% in MKN7 and MKN74) increased in comparison to the controls, suggesting that cell-cycle arrest had occurred. All of the gastric cancer cell lines were given MK4 in different concentrations and two kinds of anticancer agent, with the result that cell growth was inhibited by the anticancer agent in a dose-dependent manner when it was given with MK4 in concentrations of up to 10 microM. In conclusion, our results demonstrate that the effect of MK4 on apoptosis and cell-cycle arrest differs in differentiated (MKN7, MKN74) and undifferentiated (KATO III, FU97) gastric cancer cell lines, and that MK4 alone or with anticancer agents has an antitumor effect on gastric cancer cell lines.     

齐墩果酸诱导人白血病HL-60细胞凋亡及细胞周期阻滞

目的：探讨齐墩果酸诱导HL-60细胞凋亡作用及其对细胞周期的影响。方法：以HL-60细胞为研究对象，以不同剂量的齐墩果酸处理HL-60细胞12 h、24 h、48 h、72 h后，用MTT法观察HL-60细胞的生长抑制率；琼脂糖凝胶电泳测定DNA梯形条带；流式细胞仪分析HL-60细胞细胞周期的变化；同时用Western blotting 检测凋亡途径最终执行者caspase-3的表达。结果：齐墩果酸对HL-60细胞生长具有明显的抑制作用，其中80 μmol/L齐墩果酸作用48 h对HL-60细胞的抑制率达到50%以上，齐墩果酸诱导细胞凋亡呈明显的时间和剂量依赖性； HL-60经齐墩果酸处理48 h出现典型的DNA梯形条带；以80 μmol/L的齐墩果酸处理HL-60细胞12 h即可以使caspase-3的前体procaspase-3断裂为有活性的caspase-3；流式细胞技术检测结果表明HL-60细胞经齐墩果酸处理后细胞周期阻滞于G₁期，其中48 h和72 h分别达到63.24%和67.90%。结论：齐墩果酸可以诱导HL-60细胞凋亡，并使细胞阻滞于G₁期。     

冬凌草甲素对急性白血病HL-60细胞的增殖抑制作用及其作用机制

目的探讨冬凌草甲素对急性白血病HL-60细胞的增殖抑制作用及其作用机制。方法以不同浓度的冬凌草甲素作用于体外培养的HL-60细胞，MTr法检测细胞生长抑制率，应用流式细胞仪检测细胞凋亡情况，瑞氏染色法观察细胞凋亡时的形态学变化。应用PCR．ELISA及RT—PCR法检测细胞凋亡前后端粒酶活性及端粒酶hTERT mRNA表达水平的变化。结果冬凌草甲素可显著的抑制HL-60细胞的生长，诱导细胞发生凋亡，并呈现出明显的量-与时-效关系。冬凌草甲素作用48—60h后在瑞氏染色图片上可见核浓缩及核碎裂等典型的细胞凋亡特征，同时端粒酶hTERT mRNA的表达水平及端粒酶活性均明显降低。结论冬凌草甲素能抑制HL-60细胞的生长及诱导细胞发生凋亡：降低端粒酶hTERT mRNA的表达水平及端粒酶活性可能是其重要作用机制之一。     

Sesquiterpenes (costunolide and zaluzanin D) isolated from laurel (Laurus nobilis L.) induce cell death and morphological change indicative of apoptotic chromatin condensation in leukemia HL-60 cells

Sesquiterpenes (costunolide and zaluzanin D) were purified from laurel (Laurus nobilis L.) and identified by Mass, and 1H- and 13C-NMR. These sesquiterpenes displayed strong growth inhibitory effect against human promyelotic leukemia HL-60 cells. Apoptotic morphological changes of the nucleus, including chromatin condensation were induced in the HL-60 cells treated with the sesquiterpenes. Flow cytometric analysis showed that the hypodiploid nuclei of HL-60 cells were increased to 11.4, 47.0, and 92.5% after a 3-day-treatment with 5, 10 and 15 micro M costunolide, respectively. The same analysis showed that the hypodiploid nuclei of HL 60 cells were increased to 12.4, 28.9 and 76.7% after a 3-day-treatment with 10, 15 and 20 micro M zaluzanin D, respectively. These findings suggest that growth inhibition by costunolide and zaluzanin D of HL-60 cells results from the induction of chromatin condensation in the HL-60 cells. On the other hand, fragmentations by these compounds of DNA to oligonucleosomal-sized fragments were not observed in the HL-60 cells.     

一氧化氮诱导HL-60细胞凋亡及其机制探讨

目的：观察一氧化氮对人类白血病细胞是否具有致凋亡作用，并研究Bcl-2基因和P53基因在此过程中的作用。方法：将不同浓度的外源性一氧化氮供体亚硝基铁氰化钠与HL-60细胞作用，观察其作用的时间效应和剂量效应；用MTT法观察NO对细胞的抑制作用，用透射电镜观察细胞结构改变，用DNA凝胶电泳、细胞DNA含量、DNA末端标记、Annexin-V/PI法等分析细胞凋亡，并用流式细胞法进一步观察在NO作用过程中凋亡调控因子Bcl-2和P53蛋白及线粒体膜蛋白表达变化。结果：NO能抑制HL-60细胞生长，并在一定的剂量范围内显示作用时间和剂量的量效关系；典型的细胞形态改变、DNA片段化、亚G1峰检出、DNA末端标记、Annexin-V/PT^-表达增加等证实。NO能诱导白血病细胞凋亡；在此过程中，P53蛋白表达上调，而Bcl-2蛋白表达下调，线粒体膜蛋白表达增加。结论：NO对HL-60细胞有强的致凋亡作用，Bcl-2和P53参与NO诱导HL-60细胞凋亡的调控。     

Light-induced photoactivation of hypericin inhibits cellular growth in pituitary adenoma cell line AtT20/D16v-F2 (hypericin inhibits cellular growth of AtT20/D16v-F2)

Cultivation with 4-8 mumol/l hypericin (specific proteinkinase C inhibitor) activated by light induced high inhibition of the rate of HL-60 cell growth. When hypericin treated cells were not exposed to light growth inhibition was insignificant. Cultivation with light activated hypericin in concentration 16 mumol/l slightly inhibited growth rate of AtT20/D16v-F2 cells. AtT20/D16v-F2 cells did not proliferate in presence of light activated 32 mumol/l hypericin. Evidence of apoptosis was found in HL-60 cells treated with 1-8 mumol/l light activated hypericin, with maximum of apoptotic cells detected after 8 mumol/l light activated hypericin. Light activated hypericin induces both apoptosis and necrosis in dose and time dependent manners in HL-60 cells, but causes only necrosis in AtT20/D16v-F2 cells.     

Isolation of five types of flavonol from seabuckthorn (Hippophae rhamnoides) and induction of apoptosis by some of the flavonols in human promyelotic leukemia HL-60 cells

Five types of flavonol were isolated from seabuckthorn (Hippophae rhamnoides) and identified by mass, 1H- and 13C-NMR. The proliferations of human promyelotic leukemia HL-60 cells were inhibited as the concentrations of these flavonols were increased. The order of the extent of growth inhibition by the flavonols at a concentration of 20 microM is as follows: pentamethylquercetin > syringetin > isorhamnetin > quercetin > kaempherol > myricetin. Apoptotic morphological changes of the nucleus, including chromatin condensation were induced in the HL-60 cells treated with quercetin, kaempherol and myricetin, respectively, but not in the cells treated with the other flavonols. The fragmentations of DNA by quercetin, kaempherol and myricetin, respectively, to oligonucleosomal-sized fragments, a characteristic of apoptosis, were observed to be dose-dependent in the HL-60 cells. These findings suggest that growth inhibition by quercetin, kaempherol and myricetin, respectively, results from the induction of apoptosis by these flavonols. The other flavonols (pentamethylquercetin, syringetin and isorhamnetin) having methoxy (-OCH3) group inhibited more strongly than the above 3 flavonols without induction of apoptosis in the HL-60 cells. These findings suggest that mechanisms of growth inhibition by pentamethylquercetin, syringetin and isorhamnetin are different from the apoptosis caused by quercetin, kaempherol and myricetin.     

天花粉蛋白诱导人类白血病细胞株HL-60细胞凋亡的研究

目的:研究单链核糖体失活蛋白天花粉蛋白(TCS)诱导人类白血病细胞株HL-60细胞发生凋亡的作用及放线菌酮(CHX)对此作用的影响。方法:采用流式细胞术分析及荧光显微镜观察研究TCS诱导HL-60细胞发生凋亡的情况。结果:流式细胞术分析表明TCS能够诱导HL-60细胞发生明显的凋亡现象,TCS(20mg/L)处理48h细胞凋亡百分率为48.7%±2.3%(x±s),明显高于对照组的凋亡率(6.3%±1.0%)(P＜0.05),而CHX(5mg/L)相同条件下诱导的凋亡率为65.3%±3.9%。TCS诱导的凋亡现象进一步为荧光显微镜的观察及DNA凝胶电泳所证实,TCS处理的细胞中有许多细胞呈现典型的凋亡细胞核形态改变,如染色体凝缩、核碎裂等;DNA凝胶电泳显示TCS处理的细胞呈典型的梯级格局。进一步研究表明预先以低浓度CHX(0.2mg/L)处理可显著加强TCS的作用,而在这个浓度下单独CHX并不诱导明显的细胞凋亡。TCS诱导HL-60细胞的凋亡呈时间和剂量依赖关系。结论:TCS能够诱导HL-60细胞发生明显的凋亡,CHX可加强这种作用。这些结果提示TCS诱导的凋亡不依赖于新的蛋白质合成。     

塞来昔布减低HL-60和HL-60A细胞活力、诱导凋亡及抑制自噬

目的:探讨塞来昔布对急性髓细胞白血病(AML)HL-60细胞和HL-60A细胞的活力、凋亡及自噬的影响。方法:用不同浓度的(0、20、40、60、80和100μmol/L)塞来昔布作用于HL-60细胞和HL-60A细胞,24h、48h和72h后用MTT法检测细胞活力。用流式细胞术检测塞来昔布作用HL-60细胞和HL-60A细胞24 h后的凋亡率。用Western blot法检测凋亡相关蛋白cleaved caspase-3、cleaved PARP,自噬相关蛋白LC3、P62,以及mTOR信号途径相关蛋白。结果:塞来昔布作用于HL-60细胞24h、48h和72h的IC_(50)分别为49.4μmol/L、32.0μmol/L和25.1μmol/L,对于HL-60A细胞,相应的IC_(50)分别是69.1μmol/L、42.5μmol/L和29.6μmol/L。塞来昔布作用24h后,流式细胞术检测显示HL-60细胞中Annexin-V~+PI~-、Annexin-V~+PI~+及Annexin-V~-PI~+细胞的比例增多;HL-60A细胞中Annexin-V~+PI~-及Annexin-V~+PI~+细胞的比例增多。Western blot实验结果显示塞来昔布作用后,cleaved caspase-3和cleaved PARP的蛋白水平增高,提示该凋亡作用是通过caspase途径的。自噬相关蛋白LC3Ⅱ及P62的表达均增加,mTOR、p-mTOR以及下游的4-EBP、p-4-EBP的蛋白水平没有变化,说明塞来昔布能够抑制AML细胞自噬,该作用与mTOR途径无关。结论:塞来昔布对HL-60细胞和HL-60A细胞活力的抑制作用呈浓度以及时间依赖性,该作用与塞来昔布诱导细胞凋亡及坏死有关。塞来昔布能够通过非mTOR依赖途径抑制AML细胞自噬,有望联合应用于AML的治疗,有助于增强某些引起保护性自噬的化疗药物的细胞毒作用。     

12-O-tetradecanoyl phorbol 13-acetate, protein kinase C (PKC) activator, protects human leukemia HL-60 cells from taxol-induced apoptosis: possible role for extracellular signal-regulated kinase

The purpose of this study was to evaluate whether the mitogen-activated protein kinase / extracellular signal-regulated kinase (MEK) signaling pathway contributes to 12-O-tertadecanoyl phorbol 13-acetate (TPA)mediated protection from taxol-induced apoptosis of human leukemia HL-60 cells. Treatment of cells with taxol for 12 h resulted in apoptosis of HL-60 cells. TPA was protective against taxol-induced apoptosis and this anti-apoptotic effect was reversible when TPA was used in conjunction with staurosporine and H-7, PKC inhibitors, suggesting that TPA may protect HL-60 cells against taxol-induced apoptosis via the PKC-dependent pathway. Since TPA stimulates MEK signal transduction pathway in HL-60 cells, we postulated that MEK pathway may be playing a role in the ability of TPA to inhibit taxol-induced apoptosis. PD098059, a specific MEK kinase inhibitor, abolished the ability of TPA to inhibit taxol-induced apoptosis. These results suggest that activation of PKC in HL-60 cells confers protection against taxol-induced apoptosis and that MEK mediates anti-apoptotic signaling of PKC.     

抗人DR5单克隆抗体诱导HL-60细胞凋亡机制

探讨抗人DR5单克隆抗体(mDRA-6)诱导白血病细胞系HL-60细胞凋亡的可能机制。MTT法检测mDRA-6对HL-60细胞的生长增殖的影响,以及Caspase 8、10、3抑制剂对mDRA-6抑制HL-60细胞生长增殖的影响;琼脂糖凝胶电泳检测HL-60细胞DNA片断化降解;Western blot检测mDRA-6对HL-60细胞Caspase 8、10、3的激活改变。结果发现,mDRA-6呈时间、浓度依赖性地抑制HL-60细胞的生长增殖,10 mg/L的mDRA-6作用HL-60细胞6 h、8 h和10h,细胞增殖抑制率分别为23.96%、44.10%和50.28%;琼脂糖凝胶电泳显示,10 mg/L的mDRA-6作用6 h,HL-60细胞呈现凋亡细胞特有的DNA梯形条带;Western blot检测结果发现,mDRA-6作用HL 60细胞不同时间,Caspase 8均只有酶原条带出现,无激活片段产生,而Caspase 10和Caspase 3显示明显裂解片段产生,并随mDRA-6作用时间延长而增多;预先使用15μmol/L的Caspase 10及Caspase 3抑制剂孵育细胞1 h,能够使mDRA-6对HL-60细胞的生长抑制率分别降低64.15%(t=10.13、P<0.01)和53.69(t=8.93、P<0.01)%,而预先使用15μmol/L的Caspase 8抑制剂孵育细胞1 h,mDRA-6对HL-60细胞的生长抑制率仅降低4.40%(t=0.52、P>0.05)。以上实验结果提示,mDRA-6通过激活Caspase 10启动凋亡信号分子,诱导白血病HL-60细胞凋亡。     

WT1异构体比例转变对人白血病细胞株HL-60增殖和凋亡的影响

 目的： 探讨WT1异构体比例改变对人白血病细胞株HL-60增殖和凋亡的影响。方法： 逆转录获得人WT1(17AA－/KTS－)异构体全长cDNA序列,连接到PCDH1-MCS1-EF1-copGFP慢病毒质粒载体上, 酶切和测序证实正确构建重组质粒,建立WT1异构体表达比例改变的单克隆细胞株。MTT法检测细胞增殖活性,形态学观察及Annexin V 检测细胞凋亡。结果： 成功构建了真核表达载体PCDH1-MCS1-EF1-copGFP-WT1(17AA－/KTS－),转染HL-60细胞后,实时荧光定量RT-PCR和Western blotting 显示重组质粒转染细胞中WT1(17AA－/KTS－) mRNA和蛋白水平明显高于空质粒转染组和正常对照组。重组质粒转染细胞的生长抑制率高于空质粒转染组和正常对照组, 差异显著(P<0.05)。加2 μmol/L 三氧化二砷（As2O3）培养48 h后, 形态学观察发现3组细胞都出现了凋亡形态, 但重组质粒转染细胞更为明显。流式细胞术结果显示,As2O3作用24 h后,重组质粒转染细胞凋亡率较空质粒转染组和正常对照组细胞升高,差异显著(P<0.05)。结论： 增加外源性WT1(17AA－/KTS－)异构体的表达能抑制HL-60细胞增殖,促进As2O3 诱导的细胞凋亡。     

骨髓基质细胞HS-分泌物白细胞介素-对人急性髓细胞性白血病细胞系HL-0抗凋亡的作用

目的 探讨骨髓基质细胞HS-分泌物白细胞介素-6(IL-6)急性髓细胞性白血病（AML）细胞系HL-0增殖与凋亡的影响。方法 外培养HL-60细胞与HS-5细胞,构建共培养体系,应用扫描电子显微镜、ELISA法、细胞计数试剂盒8（CCK-8）法、AnnexinV-FITC/PI 双染流式细胞术、Real-time PCR和Western blotting技术分别检测HL-60细胞增殖和凋亡的变化;将不同组的HL-60细胞分别接种于BALB/c裸鼠,观察并记录成瘤情况。结果 骨髓基质细胞HS-5分泌的IL-6能够促进HL-60细胞增殖、抑制其凋亡,并下调HL-60细胞中的促凋亡基因Bax的表达,上调抗凋亡基因Bcl-2的表达。共培养组HL-60细胞在BALB/c裸鼠中成瘤能力最强,HL-60细胞单独培养组成瘤能力最弱。结论 骨髓基质细胞HS-5促进HL-60细胞增殖、抑制其凋亡的部分作用机制是通过分泌IL-6实现的。