藤黄酸对人结肠癌HT-29细胞生物学行为及JNK信号通路的影响

目的探讨藤黄酸对人结肠癌HT-29细胞增殖、凋亡、迁移及ASK-1、p-ASK-1、JNK、p-JNK表达的影响。方法将人结肠癌HT-29细胞分为空白对照组与藤黄酸组(0.5、1.0、2.5、5.0μmol/ml)。不同浓度藤黄酸干预24、48、72h后,MTT方法检测藤黄酸对HT-29细胞增殖的抑制作用。2.5μmol/ml藤黄酸干预48 h后,流式细胞术检测HT-29细胞的凋亡率;划痕实验检测藤黄酸对HT-29细胞迁移能力的影响;Western blot实验检测藤黄酸对HT-29细胞JNK、p-JNK、ASK-1、p-ASK-1的表达。结果不同浓度藤黄酸均能显著抑制HT-29细胞增殖,且呈时间和浓度依赖性。2.5μmol/ml藤黄酸干预48 h后,HT-29细胞凋亡率升高,迁移能力降低(P0.01);JNK、p-JNK、ASK-1、p-ASK-1蛋白表达水平均显著升高(P0.01)。结论藤黄酸能够抑制人结肠癌HT-29细胞增殖与迁移,并促进凋亡,其作用机制可能与调控JNK信号通路相关。     

过表达海兔属Ras同源物I(ARHI)增加人SW480结肠癌细胞凋亡

目的观察海兔属Ras同源物I(ARHI)对SW480人结肠癌细胞凋亡的影响。方法采用pc DNA3.1-FLAG-ARHI质粒转染和G418筛选法建立稳定表达ARHI的SW480细胞,采用反转录PCR验证ARHI mRNA和蛋白的表达。流式细胞术检测过表达ARHI对结肠癌细胞凋亡的影响;Western blot法检测蛋白激酶B(Akt)、磷酸化Akt(p-Akt)、p53和Bcl-2的蛋白水平。结果成功建立过表达ARHI的SW480细胞,过表达ARHI的SW480细胞凋亡率明显增加,Bcl-2和p-Akt蛋白水平明显降低、P53蛋白表达水平增加,而Akt蛋白水平无明显变化。结论过表达ARHI通过抑制Akt水平增加SW480人结肠癌细胞凋亡。     

敲减NOB1基因表达对人结肠癌SW480细胞药物敏感性及侵袭和迁移能力的影响

目的:探讨通过小干扰RNA(small interfering RNA, siRNA)技术敲减NOB1基因表达对人结肠癌SW480细胞活力、药物敏感性、凋亡、细胞周期及侵袭和迁移能力的影响。方法:利用脂质体Lipofectamine 3000将NOB1 siRNA转染至SW480细胞,采用real-time PCR和Western blot检测转染后SW480细胞中NOB1 mRNA和蛋白表达的变化;采用MTT法检测敲减NOB1基因表达后SW480细胞活力及其对不同化疗药物(顺铂、5-氟尿嘧啶、奥沙利铂和卡培他滨)敏感性的变化;流式细胞术检测敲减NOB1基因表达对SW480细胞凋亡和周期的影响;Transwell方法检测敲减NOB1基因表达对结肠癌SW480细胞侵袭和迁移能力的影响。结果:转染NOB1 siRNA后,SW480细胞中NOB1的mRNA和蛋白表达水平明显降低(P0.05);与对照组和阴性对照siRNA组相比,NOB1 siRNA转染组的SW480细胞在24～72 h的细胞活力显著降低,顺铂、5-氟尿嘧啶、奥沙利铂和卡培他滨对该细胞的半数抑制浓度均显著降低,细胞凋亡率显著增加,细胞周期受到阻滞,细胞侵袭和迁移能力显著降低(P0.05)。结论:NOB1 siRNA转染能够抑制结肠癌SW480细胞活力及侵袭和转移能力,并增强细胞对药物的敏感性,促进细胞凋亡。NOB1能够成为结肠癌诊断和治疗的新靶点。     

GSK-3β抑制剂对结肠癌SW480细胞增殖和凋亡的影响

目的: 探讨糖原合成酶激酶3β(GSK-3β)抑制剂(2'Z,3'E)-6-溴靛'-3'-肟(BIO)对结肠癌SW480细胞β-catenin 、Bcl-2蛋白表达及细胞周期、凋亡的影响。方法: 应用不同浓度BIO作用于结肠癌SW480细胞,采用流式细胞术检测细胞周期及凋亡,Western blotting检测β-catenin 和Bcl-2蛋白表达,免疫细胞化学检测β-catenin 及cyclin D1的表达,HE染色观察细胞形态。结果: 与BIO处理前SW480细胞相比,BIO处理组SW480细胞β-catenin蛋白表达明显上调并出现部分细胞核移位,cyclin D1蛋白表达及S期和G₂/M期细胞不同程度增多,Bcl-2蛋白表达有所下调,细胞凋亡率明显下降,并出现细胞形态改变。结论: GSK-3β抑制剂BIO作用于结肠癌SW480细胞呈现促增殖及抑凋亡作用,其机制主要与β-catenin信号转导通路激活以及与Bcl-2调控通路的平衡有关,其中β-catenin上调可能是影响结肠癌SW480细胞转归的主要因素。     

姜黄素通过抑制STAT3通路调控人结肠癌耐奥沙利铂细胞株的耐药性

目的:探讨姜黄素(Cur)对人结肠癌耐奥沙利铂(Oxa)细胞株(SW620/OxR)的逆转耐药作用及其机制是否与抑制STAT3信号通路有关。方法:采用WST-1试剂检测Cur对SW620/OxR细胞株的半数抑制(IC50)浓度,选择IC50低一浓度梯度的Cur+2μmol/L Oxa作用于SW620/OxR细胞48 h(称为实验组),与仅加入2μmol/L的Oxa对照组比较,1采用流式细胞术检测细胞凋亡;2采用Western blot检测STAT3活化标志磷酸化STAT3(P-STAT3)蛋白及其下游耐药相关靶分子P糖蛋白(P-gp)的表达情况。结果:Cur对SW620/OxR细胞的IC50浓度为18.9μmol/L;实验组与对照组比较:1细胞凋亡率由(5.08±1.82)%上升到(30.69±2.94)%,实验组细胞凋亡率明显高于对照组(P0.05);2P-STAT3及P-gp表达量均明显受抑制(P0.05)。结论:Cur具有调控人结肠癌耐药细胞株耐药性的作用,可能与抑制STAT3信号通路,降低P-gp表达有关。     

艰难梭菌毒素B诱导结肠癌细胞凋亡及相关机制研究

目的检测艰难梭菌毒素B(TcdB)对结肠癌SW480细胞增殖与凋亡的影响,研究其引起细胞凋亡的相关机制。方法采用不同浓度的TcdB处理SW480细胞,采用MTT法检测细胞增殖情况;用流式细胞术检测细胞的凋亡及线粒体膜电位变化情况。结果TcdB显著抑制了结肠癌SW480细胞的增殖,作用48 h后的抑制率为46.36%,呈一定的时间-浓度相关性;流式细胞仪检测结果表明,浓度为800 ng/ml的TcdB作用48 h,SW480细胞凋亡率为20.83%,呈一定的时间-浓度相关性。结论艰难梭菌毒素B能够抑制结肠癌SW480细胞增殖、诱导细胞凋亡,其机制可能与启动线粒体凋亡途径有关。     

肽聚糖通过TLR2诱导人绒毛外滋养细胞的凋亡及意义

目的初步研究肽聚糖通过Toll样受体2(TLR2)诱导人早孕绒毛外滋养细胞株TEV-1细胞的凋亡及其意义。方法免疫细胞化学检测TLR2蛋白在TEV-1细胞的定位表达,不同浓度肽聚糖刺激TEV-1细胞后AnnexinV/PI流式细胞术检测细胞的凋亡率。结果①TEV-1细胞表达TLR2,且定位于细胞膜和细胞浆。②30μg/ml肽聚糖刺激TEV-1细胞24小时后与对照组比较,细胞凋亡率无明显增加(8.17±0.1%,P>0.05),而刺激时间延长至48h可诱导出明显增加的细胞凋亡(16.03±1.51%,P<0.01);大剂量组80μg/ml肽聚糖刺激TEV-1细胞24h、48h均可诱导明显增加的细胞凋亡(14.13±1.06%和51.67±1.56%,P<0.01)。结论人绒毛外滋养细胞株TEV-1表达TLR2,肽聚糖可通过TLR2诱导TEV-1细胞凋亡,且存在时间和剂量依赖性,提示宫内感染时G+菌可能通过TLR2介导胎盘滋养细胞凋亡来影响妊娠的结局。     

多烯紫杉醇对人结肠癌SW480细胞增殖的影响及其机制的探讨

目的:观察多烯紫杉醇对人结肠癌SW480细胞增殖的影响及其机制探讨。方法:用不同浓度(5、10、20nmol·L-1)多烯紫杉醇处理人结肠癌SW480细胞后,采用MTT法观察多烯紫杉醇对人结肠癌SW480细胞增殖的影响,并使用流式细胞术及Hoechst33258染色检测多烯紫杉醇对SW480细胞的凋亡影响,采用RT-PCR检测SW480细胞Bcl-2mRNA表达。结果:经不同浓度(5、10、20nmol·L-1)多烯紫杉醇处理后,MTT结果显示SW480细胞生长抑制率显著上升,流式细胞术检测显示SW480细胞凋亡发生显著升高,并且Hoechst33258染色检测SW480细胞呈凋亡状态。此外,RT-PCR检测T-24细胞Bcl-2mRNA表达水平降低。结论:多烯紫杉醇通过诱导凋亡能抑制人结肠癌SW480细胞的生长,这可能与其下调Bcl-2mRNA表达有关。     

TRAIL联合氟尿嘧啶体外诱导结肠癌细胞凋亡

目的:探讨氟尿嘧啶(Fu)对重组人肿瘤坏死因子相关凋亡诱导配体(tumor necrosis factor-relatedapoptosis-inducing ligand,TRAIL)诱导结肠癌细胞凋亡的影响及其作用机制。方法:采用四甲基偶氮唑蓝比色法检测Fu及联合rmhTRAIL对人结肠癌SW480的IC50值;流式细胞术检测不同浓度Fu与rmhTRAIL联合处理SW480 24 h后细胞的凋亡率;实时荧光定量PCR和Western印迹法检测不同浓度Fu与rmhTRAIL联合处理SW480 24 h后细胞survivin基因mRNA和蛋白表达变化。结果:细胞经药物处理24 h后,单用组IC50值为29.5μmol/L,Fu联合rmhTRAIL组IC50值为6.4μmol/L,高质量浓度联合组药物相互作用系数为0.92;Fu与rmhTRAIL联合作用24 h后,随Fu质量浓度增高survivin mRNA和蛋白的表达显著下调。结论:Fu能增强TRAIL诱导的结肠癌细胞凋亡,其机制可能与下调survivin表达有关。     

miR-27a对结肠癌SW480细胞增殖、迁移、侵袭及凋亡的影响及可能机制

目的 探讨miR-27a对结肠癌SW480细胞增殖、凋亡、侵袭及迁移的影响及可能机制。方法 qRT-PCR方法检测人结肠癌细胞株SW480与人正常结肠黏膜上皮细胞NCM460中miR-27a的表达水平。体外培养SW480细胞,将SW480细胞随机分为空白对照组(不进行任何处理)、miR-27a抑制剂组（转染miR-27a inhibitor）与阴性对照组（转染miR-27a inhibitor NC）,采用脂质体法进行转染,实时荧光定量PCR方法验证转染效率。采用四甲基偶氮唑蓝（MTT）法检测SW480细胞增殖;Transwell实验检测SW480细胞侵袭与迁移;流式细胞术检测SW480细胞凋亡;Western blot法检测转染后叉头框蛋白O1(FOXO1)、组织金属蛋白酶抑制剂2(TIMP-2)、泛素连接酶FBW7的表达。结果 miR-27a在SW480细胞中的表达水平显著高于NCM460细胞（P<0.01）。转染miR-27a抑制剂后,SW480细胞中miR-27a的表达水平明显降低,转染成功。抑制miR-27a表达后,SW480细胞的增殖、迁移与侵袭能力显著降低,凋亡率显...     

RNAi双沉默Survivin和hTERT基因抑制人结肠癌SW480细胞增殖促进凋亡

目的探讨双向沉默Survivin和h TERT基因对结肠癌SW480细胞增殖和凋亡的影响,为结肠癌的基因治疗提供实验依据。方法设计并构建能够稳定转录shRNA并可分别及联合干扰Survivin和h TERT分子表达的质粒,将其转染结肠癌SW480细胞后,分阴性对照组、空白质粒对照组、Survivin RNAi组、h TERT RNAi组和Survivinh TERT RNAi组。转染48h后TRAP-PCR-ELISA法检测端粒酶活性,RT-PCR法检测Survivin和h TERT mRNA的表达,Western blot检测Survivin和h TERT蛋白的表达,流式细胞仪及cck-8法分别检测细胞凋亡和细胞增殖的变化。结果 Survivin-h TERT RNAi组SW480细胞端粒酶活性明显下降(P0.01),Survivin-h TERT RNAi组Survivin及h TERT的mRNA水平较正常对照组分别减低82.8%和73.6%(P0.01),蛋白表达抑制率分别为79.2%和66.7%(P0.01)。实验各组中Survivin-h TERT RNAi组细胞增殖抑制率和凋亡率最高,分别为43.6%±0.1%和39.2%±2.3%(P0.01)。结论 Survivin和h TERT双干扰质粒可明显下调Survivin和h TERT蛋白的表达,抑制结肠癌SW480细胞的增殖,促进其凋亡。     

Immune reactions induced by interleukin-2 transfected colorectal cancer cells in vitro: predominant induction of lymphokine-activated killer cells

One aim of the genetic modification of tumor cells is the generation of immunogenic variants that can be used for the induction of immune responses against tumors. We engineered the human colorectal carcinoma cell line SW480 by means of plasmid transfection to secrete interleukin (IL)-2. Transfection of SW480 cells resulted in stable IL-2 secretion at 5–30 ng/ml per 10⁵ cells in 24 h and, unexpectedly, in CD54 expression on the cell surface. SW480 variants expressing IL-2 and CD54 were tested for their capacity to induce T lymphocyte activation in vitro in comparison to untransfected and CD54 transfected cells. The cytolytic effector function of a class I MHC restricted CD8⁺, peptide antigen specific T cell clone was augmented following expression of CD54. IL-2 secreting SW480 variants did not further increase antigen-dependent cytolysis. Primary activation of resting T lymphocytes was assessed following allogeneic stimulation. When compared with unmodified SW480 cells, CD54 expressing variants did not initiate T cell proliferation. In contrast, IL-2 secreting SW480 cells strongly promoted primary T cell proliferation. Similarly, exogenous IL-2 and SW480 cells induced T cell pro liferatiowhich was not only due to IL-2 but was depen dent on tumor cells. However, following the initial wave of cell growth in response to IL-2 secreting SW480 cells T lymphocytes could not be restimulated with SW480 or IL-2 secreting variants and could not be further expanded. T cells initially activated by IL-2 secreting SW480 cells exhibited cytolytic activity towards SW480 cells. This reactivity, however, was transient and completely blocked by K562 cells, suggesting MHC-unrestricted, nonspecific cytotoxicity. We conclude that endogenous IL-2 secretion by the colorectal carcinoma cell line SW480 does not result in the activation of MHC restricted specific T lymphocytes but predominantly induces lymphokine-activated killer cells. Considering that tumor cell vaccines are aimed at inducing tumor-specific immune responses, our in vitro observation would rather argue against the in vivo application of such a tumor cell modification in colorectal cancer.Abbreviations IL Interleukin - LAK Lymphokine-activated killer - PBMC Peripheral blood mononuclear cells     

骨桥蛋白基因真核表达载体构建及对结肠癌细胞的作用

目的：构建骨桥蛋白（Osteopontin,OPN）基因真核表达载体,转染人结肠癌细胞SW480,分析其对SW480细胞株增殖及生存能力的作用。方法：构建重组表达载体pEGFP-N1/OPN,经测序鉴定无误后,转染人结肠癌SW480细胞。RT-PCR检测SW480细胞转染后OPN mRNA表达;Western blot检测SW480细胞转染后OPN蛋白表达量;Cell Counting Kit-8（CCK-8）测定细胞增殖;软琼脂克隆形成实验观察细胞的锚定非依赖性生长能力。结果：pEGFP-N1/OPN转染SW480后,OPN基因获得很好转录,OPN蛋白表达增高,转染OPN后SW480细胞增殖率（光吸收值）显著高于转染阴性组（P〈0.05）,软琼脂克隆形成速度增快,数量明显多于对照组和空载体组（P〈0.05）。结论：OPN基因真核表达载体pEGFP-N1/OPN构建成功,OPN具有促进SW480细胞增殖、存活的作用,为进一步研究OPN作用机制奠定了重要基础。     

人突变p27基因对大肠癌细胞生物学行为的影响

目的： 观察人突变p27基因（p27mt）对人大肠癌细胞生长的影响，探讨p27mt基因在大肠癌基因治疗中的作用及可能机制。方法： 以携带突变p27基因复制缺陷型腺病毒（Ad-p27mt）为载体，转染大肠癌细胞SW480；Western blotting方法检测p27mt蛋白的表达；细胞计数法检测p27mt对SW480细胞生长的抑制作用；用流式细胞仪检测细胞周期；用DNA片段分析法检测细胞凋亡。结果： Ad-p27mt转染SW480细胞后，p27在细胞中出现了蛋白高表达;77.96%的细胞阻滞于G₀/G₁期，而Ad-LacZ组及空白对照组分别为27.57%和25.29%；生长曲线显示Ad-p27mt对细胞生长有明显的抑制作用；DNA片段分析示p27mt基因可诱导细胞的凋亡。结论： p27mt对细胞周期有明显的阻滞作用，主要阻滞于G₀/G₁期；p27mt基因对细胞的生长抑制机制与诱导细胞凋亡和细胞周期的阻滞有关。     

体外不同比例再生肝细胞与结肠癌细胞的共培养

目的 观察体外与不同比例再生肝细胞共培养对结肠癌细胞增殖潜能及肝再生相关因子的影响.方法 70%肝切除大鼠模型术后24 h采用原位胶原酶灌流法分离获得有活性的再生肝细胞,分别以10:1(A组)、1:1(B组)与人结肠癌细胞株SW480共培养,对照组为单独培养的结肠癌细胞(C组).培养后第24和72 h,通过3H-胸腺嘧啶核苷(3H-TdR)掺人法比较各组培养后的增殖能力,并采用酶联免疫吸附试验(ELISA)检测表皮生长因子(EGF)、胰岛素样生长因子-1(IGF-1)及肝细胞生长因子(HGF)的浓度.结果 培养后24 h 3组间3H-TdR掺人率和EGF、IGF-1、HGF的浓度差异无统计学意义(P>0.05),72 h A、B两组的3H-TdR掺入率(15.9±1.4,13.2±1.5)和EGF[(722.9±55.4)ng/L,(498.2±41.5)ng/L]、IGF-1[(755.2±35.7)ng/L,(538.1±37.5)ng/L]明显高于C组(P<0.05),且A组高于B组(P<0.05).HGF的浓度在培养后第24、72小时差异均无统计学意义(P>0.05).结论 与再生肝细胞共培养的结肠癌细胞增殖能力增强,其机制可能与来自于肝细胞内的生长信号增加结肠癌细胞EGF和IGF-1的表达有关.     

LASP-1稳定转染对人结肠癌细胞株SW480细胞增殖及成瘤能力的影响

目的 探讨LIM和SH3蛋白1(LASP-1)对人结直肠癌细胞株体内外增殖能力的影响.方法 用逆转录聚合酶链反应(RT-PCR)和Western blot方法检测LASP-1在结直肠癌细胞株中的表达,筛选LASP-1不/低表达细胞株;将LASP-1 cDNA导入内源性低表达LASP-1基因的人结直肠癌细胞株SW480细胞中,同时构建带绿色荧光蛋白(CFP)的表达载体转染SW480细胞株,G418筛选抗性克降,经鉴定后利用四甲基偶氮唑盐(MTT)法检测LASP-1对细胞体外增殖的影响,通过整体成像系统观察LASP-1对细胞在裸鼠体内成瘤能力及肿瘤生长能力的影响.结果 成功构建pcDNA3-LASP-1和pEGFP-LASP-1表达载体,将其稳定转染低表达LASP-1的SW480细胞中.通过7 d连续比较,LASP-1基因的导入明显促进结直肠癌细胞的体外增殖能力.裸鼠皮下注射携带GFP的稳定细胞系,整体成像观察过表达LASP-1的细胞成瘤能力和肿瘤生长速度均强于对照细胞.结论 LASP-1基因具有促进结直肠癌细胞增殖的能力,可能作为结直肠癌发生过程中一个有价值的指标.

Abstract：

Objective To investigate the effect of LIM and SH3 protein 1 (LASP-1)expression on the proliferative ability of human colorectal cancer cells in vitro and in vivo. Methods RT-PCR and Western blot were used to screen cells of the colorectal cancer cell line with no or with minimal endogenous LASP-1 expression. LASP-1 cDNA with or without GFP was transfected into SW480 colorectal cancer cells with minimal LASP-1 expression. Stable transfectants were established after G418 selection. Cell proliferative capacity was assessed by MTT assay. Tumor growth was visualized by whole-body imaging system. Results pcDNA3-LASP-1 and pEGFP-LASP-1 vectors were successfully constructed and transfected into the SW480 cells. After comparative study for 7 days, LASP-1 over-expression was found capable of enhancing signific antly the proliferation of colorectal cancer cells in vitro. Stable transfectants with GFP expression were inoculated subcutaneously into the nude mice. Tumorigenesis and proliferation ability of LASP-1-overexpressed transfectants were higher than those of the control cells. Conclusion LASP-1 gene expression enhances proliferation of colorectal cancer cells and may serve as a useful marker for colorectal cancer progression.     

Generation and preliminary characterization of an antibody library with preferential reactivity to human colorectal cancer cells as compared to normal human blood cells

We are developing recombinant polyclonal antibody libraries (PCALs) reactive to human colorectal cancer cells as an anti-cancer therapeutic approach. To test the hypothesis that PCALs with preferential recognition of tumor cells as compared to normal cells could be generated, a Fab phage display library reactive to human colorectal cancer cell lines was absorbed with normal human blood cells. ELISA analysis of the absorbed Fab phage display library showed that 70% of tested clones reacted to colorectal cancer cells. Reactivity of the library to blood cells was reduced 4-10-fold, with many clones unreactive to one or more of the blood cell types. DNA fingerprint analysis of colorectal cancer-binding clones showed that the absorbed library remained polyclonal. The H and L chain V region gene pairs of the absorbed library were transferred in mass from the Fab phage display vector to a mammalian vector and expressed as IgG following transfection into Sp2/0 myeloma cells. ELISA analysis showed that 79% of transfectants expressed IgG and of those 74% were positive for binding to the SW480 human colorectal cancer cell line. A template of 95 SW480-reactive wells was assembled, designated Lib-Col2.1, and IgG purified from a consolidated mass culture. The purified Lib-Col2.1 IgG was compared to the clinically used anti-colorectal cancer mAb 17-1A, by ELISA and flow cytometry, for binding density on SW480 colorectal cancer cells and on normal human blood cells. The results showed that Lib-Col2.1 bound to SW480 cells at higher density than mAb 17-1A and that its binding to normal human blood cells was reduced 2.4-24-fold relative to an unabsorbed anti-SW480 serum. Furthermore, Lib-Col2.1 was more effective than mAb 17-1A at inhibiting the growth of SW480 cells in culture. These results suggest that a polyclonal antibody library with preferential reactivity to cancer cells as compared to normal cells could be generated.     

TIPE3 干扰质粒对SW480 结肠癌细胞生长的作用及相关机制探讨

目的:通过TIPE3 干扰质粒转染SW480 结肠癌细胞,验证干扰TIPE3 表达对SW480 结肠癌细胞生长的影响并探讨相关机制。方法:构建TIPE3-shRNA-pSIREN-RetroQ 干扰质粒,通过脂质体转染法成功将干扰质粒导入SW480 细胞,通过RT-PCR、Western blot 检测重组质粒的干扰效率。应用CCK-8 方法检测SW480 细胞生存率。AnnexinV-FITC/ PI 流式细胞法检测细胞凋亡。使用Western blot 检测细胞增殖、凋亡相关分子的表达情况。结果:成功设计、构建和筛选具有生物活性且干扰效率最佳的TIPE3-shRNA-pSIREN-RetroQ 干扰质粒。CCK-8 检测证实干扰SW480 结肠癌细胞TIPE3 表达可以抑制细胞生长。流式结果显示,TIPE3-shRNA3 干扰组的凋亡率为(27.99±1.087)%,显著高于正常细胞组(12.10±2.213)% 及转染空载质粒组(11.44±0.277 0)%。证实了降低TIPE3 表达可以增加SW480 对aDR5ScFv 所诱导的细胞凋亡敏感性。Western blot结果显示干扰TIPE3 表达可以活化caspase3 蛋白,降低p-AKT、p-PDK1、PCNA 等分子的表达。结论:干扰TIPE3 的表达对 SW480 结肠癌细胞具有促进凋亡,抑制增殖的作用。