Wnt信号传导通路在塞来昔布抗结肠癌生长中的作用

目的 研究Wnt信号传导通路在塞来昔布抗结肠癌生长中的作用.方法 将人结肠癌HT-29细胞注射于裸鼠背部皮下建立移植瘤模型,16 d后,将裸鼠随机分为对照组、低、中和高剂量塞来昔布组(25、50和100 mg·kg-1·d-1),对照组灌胃给予灭菌蒸馏水,各塞来昔布组给予相应剂量的塞来昔布.给药35 d后,以免疫组织化学方法 检测瘤组织COX-2蛋白表达,以TUNEL方法 检测细胞凋亡,以Western印迹方法 检测凋亡抑制蛋白生存素(survivin)和β连接素(β-catenin)蛋白的表达.结果 低、中和高剂量塞来昔布组的抑瘤率分别为34.94%、39.20%和59.20%,与对照组比较,塞来昔布各组移植瘤体积明显缩小(P＜0.05),各组COX-2、survivin和β-catenin蛋白表达水平均明显降低(均P＜0.05).塞来昔布对肿瘤生长、细胞凋亡、COX-2和survivin表达的影响程度随用药剂量的增加而增强.结论 不同剂量的塞来昔布均能明显抑制结肠癌移植瘤的生长,其抑制作用呈明显的剂量依赖性,这种作用是通过COX-2依赖或非依赖途径对Wnt信号通路的抑制来诱导细胞凋亡实现的.低剂量塞来昔布是临床治疗的较好选择.     

塞来昔布干预对人胃癌细胞E-钙黏蛋白和基质金属蛋白酶-2表达的影响

目的探讨COX-2与E-cadherin、MMP-2之间的相互关系及其参与胃癌细胞侵袭迁移的可能机制。方法应用塞来昔布(celecoxib)对体外培养的人胃癌细胞SGC7901进行干预,采用实时荧光定量反转录PCR检测COX-2、E-cadherin、MMP-2 mRNA的表达;运用免疫荧光标记法结合激光共聚焦荧光显微镜分析E-cadherin的蛋白表达量;应用Transwell法检测细胞侵袭及迁移能力的变化。结果塞来昔布明显抑制体外培养的人胃癌细胞SGC-7901中COX-2 mRNA的表达,E-cadherin mRNA的表达随着COX-2的表达下降而呈浓度与时间依赖性升高,MMP-2 mRNA的表达随着COX-2的表达下降而呈浓度与时间依赖性降低。塞来昔布30μmol/L干预人胃癌细胞SGC7901 24、36、48 h后,激光共聚焦荧光显微镜检测E-cadherin的蛋白表达量明显升高。塞来昔布干预组细胞穿过Transwell小室的细胞数明显少于对照组。结论 COX-2特异性抑制剂塞来昔布通过抑制COX-2的表达,上调E-cadherin的表达,下调MMP-2的表达,抑制体外培养的胃癌细胞SGC7901的侵袭迁移能力。     

普伐他汀对人结肠癌细胞增殖及COX-2蛋白表达的影响

目的体外观察普伐他汀对人结肠癌细胞HT-29、Ls-174-T细胞增殖、细胞周期及COX-2蛋白表达的影响。方法采用噻唑蓝（MTT）法观察普伐他汀对HT-29和Ls-174-T细胞增殖的影响，流式细胞仪（FCM）研究普伐他汀对细胞周期的作用，免疫细胞化学观察COX-2蛋白的表达。结果体外普伐他汀可抑制HT-29和Ls-174-T细胞增殖，各处理组内G0／G1期细胞增多，但诱导凋亡不明显，体外普伐他汀可减少HT-29和Ls-174-T细胞株COX-2蛋白的表达。结论体外普伐他汀对HT-29和Ls-174-T细胞增殖有抑制作用，该作用可能与使细胞生长阻滞于G0／G1期及抑制COX-2蛋白表达有关。     

氧化苦参碱诱导人结肠癌SW480细胞凋亡的机制

目的探讨氧化苦参碱诱导人结肠癌SW480细胞凋亡的作用及机制。方法以不同剂量的氧化苦参碱作用于人结肠癌细胞株SW480,四甲基偶氮唑蓝法(MTT)检测细胞的增殖能力,Hoechst 33258染色法观测细胞凋亡。免疫印迹法测定B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)的表达,荧光法测定半胱氨酸蛋白酶(caspase)-3的活性。结果氧化苦参碱可剂量依赖性地抑制细胞的增殖,促进细胞凋亡。Western印迹方法显示氧化苦参碱可抑制抗凋亡蛋白Bcl-2的表达,提高促凋亡蛋白Bax的表达,同时激活凋亡效应分子caspase-3。结论氧化苦参碱能够抑制结肠癌SW480细胞的增殖,通过提高Bax的表达、抑制Bcl-2的表达、激活caspase-3发挥其诱导细胞凋亡的作用。     

选择性环氧合酶-2抑制剂塞来昔布对胃癌治疗作用的体内实验研究

目的探讨选择性环氧合酶-2(COX-2)抑制剂塞来昔布对体内胃癌生长的影响及作用机制。方法建立裸鼠胃癌模型,20只裸小鼠随机分为2组,对照组隔日腹腔注射生理盐水,塞来昔布组隔日腹腔注射塞来昔布30mg/kg,采用免疫组化法检测微血管密度(MVD),采用半定量-TRAP银染法检测端粒酶活性,流式细胞仪检测细胞周期、细胞凋亡率。结果塞来昔布组肿瘤生长明显受抑制,抑瘤率为61.3%,与对照组相比,差异有显著性(P<0.05);流式细胞仪检测到凋亡峰,细胞阻滞于G0/G1期。同时它也显著抑制胃癌细胞的端粒酶活性,肿瘤组织中的MVD较对照组显著降低。结论塞来昔布通过诱导细胞凋亡,降低端粒酶活性,减少血管生成,从而抑制胃癌生长。这可能是COX-2抑制剂塞来昔布体内抗胃癌的机制。     

选择性COX-2抑制剂塞来昔布对肝星状细胞增殖及活化的影响

目的通过观察选择性COX-2抑制剂塞来昔布对肝星状细胞增殖及活化的影响,以探讨COX-2在肝纤维化中的作用。方法用不同浓度的选择性COX-2抑制剂塞来昔布作用于体外培养的人肝星状细胞株LI-90,采用MTT法和半定量RT-PCR法检测塞来昔布对肝星状细胞增殖及活化的影响。结果塞来昔布可显著抑制体外培养的肝星状细胞LI-90的增殖和活化,随着药物剂量的增加和时间的延长,肝星状细胞LI-90的增殖和活化明显抑制,呈剂量和时间依赖性。结论塞来昔布对肝星状细胞增殖和活化的抑制作用是研究肝纤维化预防和治疗的重要方向之一。     

COX-2与卵巢癌的相关性研究进展

环氧化酶（COX）是前列腺素H2合成的限速酶,在花生四稀酸转变成前列腺素（PGS）的过程中发挥着重要作用,包括COX-1和COX-2两种同工酶。研究发现。COX-2与绝大多数恶性肿瘤的发生发展有关。现将其与卵巢癌的相关性研究进展情况综述如下。     

姜黄素对人结肠癌细胞SW480作用的体外实验研究

目的 研究姜黄素促进人结肠癌细胞系SW480凋亡的作用.方法 人结肠癌细胞系SW480与不同浓度的姜黄素共孵育48 h,MTT法检测细胞存活率,并用相差显微镜观察细胞形态学改变.用流式细胞术(检测细胞凋亡相关指标Annexin V/PI)和Ho-echst3258染色检测细胞凋亡.结果 姜黄素能够不同程度地抑制人结肠癌细胞系SW480的生长.姜黄素对SW480细胞的IC50(半数抑制浓度)为65 mg/mL.Hoechst3258荧光染色与流式细胞术分析SW480细胞的结果一致.结论 姜黄素可促进SW480细胞凋亡,为姜黄素治疗结肠癌提供依据.     

塞来昔布对大鼠溃疡性结肠炎的作用

目的观察塞来昔布对三硝基苯磺酸(TNBS)灌肠诱发结肠炎的大鼠的血清前列腺素E2(prostagland E2,PGE2)及结肠组织COX-2水平影响,并探讨塞来昔布对溃疡性结肠炎(ulcerative colitis,UC)的作用及作用机制。方法 Wistar雄性大鼠40只,随机分成4组,每组10只,A组为正常对照组(未经任何处理)、B组为水杨酸偶氮磺胺吡啶(salicylazosulfapyridine,SASP)组、C组为塞来昔布组、D组为模型对照组(0.9%氯化钠注射液)。B、C、D三组均采用TNBS/乙醇灌肠制作大鼠UC模型后,B组SASP 200 mg/kg、C组塞来昔布10 mg/kg、D组0.9%氯化钠注射液1 ml每天灌胃给药1次,连续治疗7 d后处死所有存活大鼠。在造模成功后每天评定各组大鼠一般状况、DAI(disease activity index)评分;药物治疗后第7天在全麻下心脏采血,采用酶联免疫吸附法(ELISA)检测血清PGE2浓度,取病变组织行HE染色和COX-2免疫组织化学染色。结果 B组和C组一般情况及消化道症状好于D组。C组DAI评分高于B组(P<0.01),与D组相接近(P=0.418),无显著性差异。A组(75.28±7.55)血清PGE2含量表达量均明显少于其他三组(P<0.05)。C组血清PGE2含量表达少于B组、D组(P<0.01)。结论塞来昔布对TNBS诱导的UC无明显治疗作用。虽然塞来昔布可以使TNBS诱发的肠炎大鼠结肠病变处的炎症减轻,使血清PGE2等炎症相关因子表达减少,但未能明显减轻UC肠黏膜的损害,甚至有加重疾病症状的倾向,因此,塞来昔布能否用于UC的治疗仍然有待进一步研究。     

沙利度胺对人结肠癌小鼠移植瘤放射敏感性的影响及其机制

目的探讨沙利度胺对人结肠癌小鼠移植瘤放射敏感性的影响及其协同作用的机制。方法建立Colon26肠癌小鼠移植瘤模型,将28只小鼠随机分为对照组、单纯放疗组(R组)、单纯沙利度胺组(T组)、放疗联合沙利度胺组(T+R组)。自治疗当日起,次日测量肿瘤体积,计算肿瘤抑制率,并将小鼠断髓处死后剥离瘤体,采用免疫组织化学法对各肿瘤组织中微血管密度(MVD)进行测量。结果治疗前各组小鼠移植瘤体积之间差异均无统计学意义(P0.05);肿瘤体积随治疗时间的延长逐渐变大,对照组小鼠明显大于另外三组(P0.05);其中T+R组小鼠移植瘤体积增长最慢,肿瘤生长曲线最为平缓。治疗结束时,各实验组小鼠移植瘤体积均明显小于对照组(P0.05);与对照组相比,T组、R组、T+R组抑制率分别为42.1%、47.3%、62.0%。对照组MVD数量最多,分布密集度最高;T+R组MVD数量最少,坏死区域面积最大,移植瘤组织中的MVD表达明显低于另外三组(P0.05)。结论沙利度胺能够有效增强结肠癌小鼠移植瘤的放射敏感性,其可能机制与抑制移植瘤血管的生成有关。     

Chitooligosaccharides promote radiosensitivity in colon cancer line SW480

AIM: To investigate the anti-proliferation and radiosensitization effect of chitooligosaccharides(COS) on human colon cancer cell line SW480.METHODS: SW480 cells were treated with 0, 1.0, 2.0, 3.0, 4.0 and 5.0 mg/m L of COS for 48 h. CCK-8 assay was employed to obtain the cell survival ratio of SW480 cells, and the anti-proliferation curve was observed with the inhibition ratio of COS on SW480 cells. The RAY + COS group was treated with 1.0 mg/m L of COS for 48 h, while both the RAY and RAY+COS groups were exposed to X-ray at 0, 1, 2, 4, 6 and 8 Gy, respectively. Clonogenic assay was used to analyze cell viability in the two groups at 10 d after treatment, and a cell survival curve was used to analyze the sensitization ratio of COS. The RAY group was exposed to X-ray at 6 Gy, while the RAY+COS group was treated with 1.0 mg/m L of COS for 48 h in advance and exposed to X-ray at 6 Gy. Flow cytometry was employed to detect cell cycle and apoptosis rate in the non-treatment group, as well as in the RAY and RAY + COS groups after 24 h of treatment.RESULTS: COS inhibited the proliferation of SW480 cells, and the inhibition rate positively correlated with the concentration of COS(P 0.01). Cell viability decreased as radiation dose increased in the RAY and RAY+COS groups(P 0.01). Cell viabilities in the RAY+COS group were lower than in the RAY group at all doses of X-ray exposure(P 0.01), and the sensitization ratio of COS on SW480 cells was 1.39. Compared with the non-treatment group, there was a significant increase in apoptosis rate in both the RAYand RAY + COS groups; while the apoptosis rate in the RAY+COS group was significantly higher than in the RAY group(P 0.01). In comparing these three groups, the percentage of G2/M phase in both the RAY and RAY + COS groups significantly increased, and the percentage of the S phase and G0/G1 phase was downregulated. Furthermore, the percentage in the G2/M phase was higher, and the percentage in the S phase and G0/G1 phase was lower in the RAY + COS group vs RAY group(P 0.01). CONCLUSION: COS can inhibit the proliferation of SW480 cells and enhance the radiosensitization of SW480 cells, inducing apoptosis and G2/M phase arrest.     

新霉素抑制促胃液素促人结肠癌细胞株SW480增殖的研究

目的观察新霉素（ＮＭ）对五肽促胃液素（ＰＧ）促人结肠癌细胞株ＳＷ４８０增殖的影响,探讨肌醇脂质信号通路可能参与的作用及临床意义．方法ＭＴＴ比色分析法检测活细胞数（ＶＣＣ）;［３Ｈ］肌醇标记细胞进行三磷酸肌醇（ＩＰ３）分析;Ｃａ２＋荧光测定技术检测细胞内Ｃａ２＋浓度;［γ３２Ｐ］ＡＴＰ掺入法测定蛋白激酶Ｃ（ＰＫＣ）活性．结果ＰＧ＋ＮＭ组的ＳＷ４８０细胞活细胞数降低,与对照组相比Ｐ＜００１,与ＰＧ组相比Ｐ＜００１;ＰＧ＋ＮＭ组细胞内ＩＰ３,Ｃａ２＋浓度降低,与ＰＧ组相比Ｐ＜００１,与对照组相比Ｐ＞００５;ＰＧ＋ＮＭ组膜ＰＫＣ活性降低,与ＰＧ组相比Ｐ＜００５,与对照组相比Ｐ＞００５．结论ＮＭ可能通过肌醇质脂信号通路而抑制ＰＧ促人结肠癌细胞株ＳＷ４８０的增殖,这将为结肠癌的抗信息传导治疗提供实验依据．     

桩蛋白表达下调对结直肠癌细胞SW480侵袭力的影响

目的:探讨下调桩蛋白(paxillin)的表达对结直肠癌细胞SW480体外侵袭的影响.方法:筛选常见结直肠癌细胞株中paxillin 的表达,发现SW480中表达最多.构建干扰paxillin表达的特异性短发夹RNA(shRNA),转染结直肠癌细胞SW480.将SW480细胞分为3组:正常SW480组、阴性对照组及pa...     

利培酮抑制结肠癌细胞株SW480生长的作用机制

目的:探讨利培酮对人结肠癌细胞株SW480生长抑制的作用机制及其相关研究.方法:表皮生长因子和利培酮单独或联合作用于SW480细胞,通过蛋白印迹实验观察蛋白激酶B(protein kinase B,PKB)及细胞外信号调节激酶1/2(extracellular signal-regulated kinase1/2,ERK1/2)磷酸化程度,利用RT-PCR判断细胞因子信号转导抑制因子基因表达水平,利用显微镜及细胞计数方法判断细胞生长情况.结果:利培酮抑制人表皮生长因子诱导的结肠癌细胞株SW480细胞的生长;其机制是通过激活ERK1/2的活性并诱导SOCS3的基因的表达,从而抑制PKB的磷酸化,最终抑制SW480的生长.结论:利培酮具有抑制表皮生长因子对人结肠癌细胞株的生长作用.     

Anti-proliferation effect of zoledronic acid on human colon cancer line SW480

Objective: To investigate the anti-proliferation effect and mechanism of zoledronic acid(ZOL) on human colon cancer line SW480. Methods: SW480 cells were treated with 0, 12.5, 25, 50, 100 and 200 μmo L/L of ZOL for 48 h, and CCK-8 assay was employed to obtain the survival rate of SW480 cells. SW480 cells were treated with 25 μmo L/L of ZOL for 0, 12, 24, 48 and 72 h, and then the survival rate was obtained. SW480 cells of the ZOL group were treated with 25 μmo L/L of ZOL for 48 h, while cells of the Cs A+ZOL group were pretreated with 10 μmo L/L of Cs A for 0.5 h and then treated with 25 μmo L/L of ZOL for 48 h. Then the survival rates of SW480 cells of the control group, ZOL group and Cs A+ZOL group were determined. Flow cytometry was employed to detect the apoptosis rate and the mitochondrial transmembrane potential(△ψm) of the three groups and Western blot was used to detect the expressions of cyt C in the cytosol of the three groups. Results: ZOL inhibited the proliferation of SW480 cells, and the inhibition rate positively correlated with the concentration of ZOL and the action time(P 0.01). The cell survival rate and the △ψm of the ZOL group were greatly lower than those of the control group, while the apoptosis rate and the expression of cyt C in the cytosol were obviously higher than those of the control group. All the differences showed distinctly statistical significances(P 0.01). The cell survival rate and the △ψm of the Cs A+ZOL group were all lower than those of the control group, but substantially higher than those of the ZOL group; while the apoptosis rate and the expression of cyt C in the cytosol were higher than those of the control group, but distinctly lower than those of the ZOL group. All the differences were statistically significant(P 0.01). Conclusions: ZOL can induce the apoptosis in human colon cancer line SW480 and then inhibit the proliferation of SW480 cells directly by opening the mitochondrial permeability transition pore abnormally, decreasing △ψm, and releasing the cyt C into the cytosol. And the effect enhances with the increases of the concentration of ZOL and the action time.     

RNAi对结肠癌SW480细胞Nucleostemin基因表达的影响

目的:探求RNA技术干扰人结肠癌SW480细胞Nucleostemin(NS)基因后,结肠癌SW480细胞NucleosteminmRNA和蛋白水平的表达,及细胞增殖情况变化.方法:构建Nucleostemin特异性真核表达载体,和脂质体共同转染SW480细胞后,采用Real-timePCR和Westernblot方法检测NS基因mRNA和蛋白变化,MTT法检测细胞的增殖情况.结果:与对照组相比较,RNAi干扰细胞后NSmRNA表达明显下降;NS蛋白表达亦明显下降(1.069±0.368,1.003±0.313,1.901±0.817,P<0.05;1.069±0.368,1.003±0.313,2.035±0.665,P<0.05),空白对照组(仅加入脂质体)和阴性对照组(RNAi错义序列)间无显著差异(2.035±0.665,1.9001±0.817,P>0.05).MTT显示RNA干扰后细胞增殖明显受到抑制.结论:通过特异性RNA干扰NS基因后,结肠癌SW480细胞增殖受到抑制.     

片仔癀对人结肠癌SW480细胞株的抑制作用研究

目的探究片仔癀对人结肠癌SW480细胞株的抑制效果。 方法通过对人结肠癌SW480细胞株常规体外培养,随机设定空白组、5-氟尿嘧啶（5-FU）组和不同浓度片仔癀组,分别采用对应药物干预24 h、48 h、72 h,并通过细胞增殖活力检测法（MTT法）和荧光显微镜观察其抑制效果。采用人结肠癌SW480细胞株建立结肠癌小鼠模型,把造模成功的150只小鼠随机分为模型组,5-FU组和片仔癀低、中、高剂量组,每组30只;分别以不同剂量药物外敷3 d,通过抑瘤率和原位凋亡检测（TUNEL法）解释抑制效果。 结果1 mg/mL、2 mg/mL、3 mg/mL浓度片仔癀对人结肠癌SW480细胞体外抑制率最高,为70.05%、71.39%、70.12%,与5-FU组比较差异具有统计学意义（χ²=4.49,4.97,4.52;均P<0.05）。4 mg/mL片仔癀抑制率为67.39%,与5-FU组比较差异无统计学意义（χ²=3.57,P>0.05）;荧光显微镜显示5-FU组与片仔癀各组人结肠癌SW480细胞株数量均显示不同程度的减少、体积变小、折光性差、细胞悬浮及脱落死亡。片仔癀高、中、低剂量组对人结肠癌SW480细胞的体内抑瘤率分别为51%、39%、23%,其中高、中剂量组与5-FU组比较差异无统计学意义（χ²=0.05,0.49;均P>0.05）,低剂量组与之比较差异有统计学意义（χ²=4.09,P<0.05）;荧光显微镜显示片仔癀各剂量组和5-FU组对人结肠癌SW480细胞均有不同程度的凋亡反应。 结论片仔癀外用对人结肠癌SW480细胞生长有明显的抑制作用,高、中剂量体内抑制作用与5-Fu相近,优于低剂量,临床可考虑采用高剂量可能取得更佳效果,体外抑制作用上显示则优于5-Fu,但剂量差异影响不大。     

Synergistic antitumor effect of TRAIL and doxorubicin on colon cancer cell line SW480

AIM: TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) has been reported to specifically induce apoptosis of cancer cells although only a small percentage of cell lines were sensitive to it. Cell lines not responding to TRAIL in vitro were said to be more prone to apoptosis when TRAIL was combined with another anticancer agent.Generally, factors affecting drug-sensitivity involve many apoptosis-related proteins, including p53. The expression of wild-type p53 gene was proposed as an important premise for tumor cells responding to chemotherapy. The present study was to investigate the cell killing action of TRAIL on colon cancer cell line SW480, its synergistic effect with doxorubicin, and the possible mechanisms.METHODS: SW480 cells were cultured in the regular condition and incubated with different levels of agents.Morphologic changes in these cells after treatment were observed under phase-contrast microscope and cytotoxicity by TRAIL alone and in combination with doxorubicin was quantified by a 1-day microculture tetrazolium dye (MTT) assay. In addition, flow cytometry assay (FCM) and transmission electron microscopy were used to detect apoptosis among these cells. Variation of p53 protein level among different groups according to concentrations of agents was measured by Western blot assay.RESULTS: (1) SW480 cells were not sensitive to TRAIL,with IC50&gt;l mg&#183;L^1 and dose-independent cytotoxicity. (2)SW480 cells were sensitive to doxorubicin at a certain degree,with dose-dependent cytotoxicity and IC50=65.25&#177;3.48μmol&#183;L^-1. (3) TRAIL could synergize with doxorubicin to kill SW480 cells effectively, which was represented by the boosted killing effect of doxorubicin on theses cells. IC50 of doxorubicin against SW480 cells sharply reduced when it was combined with TRAIL. (4) Subtoxic TRAIL (100 μg&#183;L^-1),combined with subtoxic doxorubicin (0.86 μmol&#183;L^-1), could kill SW480 cells sufficiently. Cytotoxicity by MTT assay arrived at 80.12&#177;2.67 %, which was significantly higher than that by TRAIL or doxorubicin alone, with P=0.006 and 0.003 respectively. This killing effect was partly due to apoptosis. It was proved by large amounts of apoptotic cells under phase-contrast microscopy, cell apoptosis rate of 76.82&#177;1.93 % by FCM assay and typical apoptotic morphology observed through transmission electron microscopy. Increase of apoptosis after combined treatment had no relation with protein level of p53 (p&gt;0.05).CONCLUSION: SW480 cells are not sensitive to TRAIL, but TRAIL can synergize with lower concentra~on of doxorubidn to induce apoptosis effectively. The status of p53 protein is not involved in the mechanism of synergistic apoptosis. It suggests the potential therapeutic applicability of the combination of TRAIL with doxorubidn against colon cancers.     

Synergistic antitumor effect of TRATL and doxorubicin on colon cancer cell line SW480

AIM: TRAIL (tumor necrosis factor-related apoptosisinducing ligand) has been reported to specifically induce apoptosis of cancer cells although only a small percentage of cell lines were sensitive to it. Cell lines not responding to TRAIL in vitro were said to be more prone to apoptosis when TRAIL was combined with another anticancer agent.Generally, factors affecting drug-sensitivity involve many apoptosis-related proteins, including p53. The expression of wild-type p53 gene was proposed as an important premise for tumor cells responding to chemotherapy. The present study was to investigate the cell killing action of TRAIL on colon cancer cell line SW480, its synergistic effect with doxorubicin, and the possible mechanisms. METHODS: SW480 cells were cultured in the regular condition and incubated with different levels of agents.Morphologic changes in these cells after treatment were observed under phase-contrast microscope and cytotoxicity by TRAIL alone and in combination with doxorubicin was quantified by a 1-day microculture tetrazolium dye (MTT)assay. In addition, flow cytometry assay (FCM) and transmission electron microscopy were used to detectapoptosis among these cells. Variation of p53 protein level among different groups according to concentrations of agents was measured by Western blot assay.RESULTS: (1) SW480 cells were not sensitive to TRAIL,with IC50＞1 mg@L1 and dose-independent cytotoxicity. (2)SW480 cells were sensitive to doxorubicin at a certain degree,with dose-dependent cytotoxicity and IC50=65.25+3.48μmol@L-1. (3) TRAIL could synergize with doxorubicin to kill SW480 cells effectively, which was represented by the boosted killing effect of doxorubicin on theses cells. IC50 of doxorubicin against SW480 cells sharply reduced when it was combined with TRAIL. (4) Subtoxic TRAIL (100 μg.L-1),combined with subtoxic doxorubicin (0.86 μmol@L1), could kill SW480 cells sufficiently. Cytotoxicity by MTT assay arrived at 80.12+2.67%, which was significantly higher than that by TRAIL or doxorubicin alone, with P=0.006 and 0.003 respectively. This killing effect was partly due to apoptosis. It was proved by large amounts of apoptotic cells under phase-contrast microscopy, cell apoptosis rate of 76.82±1.93 % by FCM assay and typical apoptotic morphology observed through transmission electron microscopy. Increase of apoptosis after combined treatment had no relation with protein level of p53 (P＞0.05). CONCLUSION: SW480 cells are not sensitive to TRAIL, but TRAIL can synergize with lower concentration of doxorubicin to induce apoptosis effectively. The status of p53 protein i snot involved in the mechanism of synergistic apoptosis. It suggests the potential therapeutic applicability of the combination of TRAIL with doxorubicin against colon cancers.