M ETTL3促进HT29和LOVO细胞增殖和迁移的实验研究

目的 研究甲基转移酶样蛋白3(methyltransferase like 3,METTL3)在结直肠癌(colorectal cancer,CRC)组织及细胞系中表达及其对HT29和LOVO细胞增殖和迁移能力的影响.方法 应用GE02R软件分析METTL3在Gene Expression Omnibus(GEO)数据...     

PXMP4促进结直肠癌细胞增殖、迁移和侵袭

目的 探讨过氧化物酶体膜蛋白4(peroxisomal membrane protein 4,PXMP4)对结直肠癌细胞增殖、迁移和侵袭能力的影响.方法 采用生物信息学分析65例配对结直肠癌组织中PXMP4 mRNA的表达.应用免疫组化检测112例配对结直肠癌组织中PXMP4的表达,并进行临床病理相关分析;利用RT-P...     

CHRDL1 调节结直肠癌增殖、 迁移和侵袭

目的 探讨腱蛋白样蛋白 1 (chordin-like 1, CHRDL1) 对结直肠癌 (colorectal cancer, CRC) 进 展的调节作用。 方法 数据库分析 CHRDL1 与 CRC 进展、 预后关系, 构建 CHRDL1 过表达 SW480、 HT29 细胞系并检测细胞增殖、 迁移和侵袭, 体外移植瘤实验检测肿瘤生长, 分析 CHRDL1 过表达对 CRC 细胞迁 移和侵袭作用机制。 结果 CHRDL1 在 CRC 进展中呈高表达且可影响预后。 CHRDL1 过表达可促进细胞增 殖、 迁移、 侵袭和移植瘤生长, 促进 Vimentin、 N-Cadherin、 snail 表达, 抑制 E-Cadherin 表达, CHRDL1 与 snail 存在互作关系, 干扰 snail 表达可逆转上述指标趋势。 结论 CHRDL1 可促进 CRC 细胞增殖, 还可通 过 Snail 促进 CRC 细胞上皮间质转化来发挥促进细胞迁移、 侵袭作用。     

微小RNA-1273g-3p对人结直肠癌HCT116和SW480细胞增殖和迁移的影响

目的:探讨微小RNA(MicroRNA,miR)-1273g-3p对结直肠癌细胞增殖和迁移的调控作用.方法:将miR-1273g-3p模拟物分别转染人结肠癌细胞(Human colon cancer cell,HCT116)和人结肠腺癌细胞(Human colon adenocarcinoma,SW480)细胞株,通过聚合酶链反应(Polymerase chain reaction,PCR)测定miR1273g-3p的表达情况;四唑盐(Methyl thiazolyl tetrazolium,MTT)比色法检测miR-1273g-3p对细胞增殖的作用;Transwell实验检测细胞的迁移能力.结果:转染miR-1273g-3p模拟物后,结直肠癌HCT116和SW480细胞miR-1273g-3p相对表达量明显上调;MTT和Transell实验结果显示,过表达miR-1273g-3p能明显促进HCT116和SW480细胞的增殖和迁移(P<0.01).结论:miR-1273g-3p具有促进结直肠癌HCT116和SW480细胞株增殖和迁移的作用.     

长链非编码RNA EVADR促进人结直肠癌细胞系增殖及迁移

目的探讨lncRNA EVADR对人结直肠癌HCT116和LOVO细胞系的增殖和迁移的影响以及其作用机制。方法利用慢病毒感染方式分别构建稳定过表达lncRNA EVADR的HCT116和LOVO细胞系;用CCK-8检测细胞的增殖;Transwell小室法检测细胞迁移能力,Western blot检测E-cadherin的表达,实时荧光定量PCR检测Snail、Slug、ZEB1和ZEB2 mRNA的表达。结果成功构建了稳定过表达lncRNA EVADR的结直肠癌HCT116和LOVO细胞系。与HCT116-NC和LOVO-NC细胞组对比,HCT116-EVADR与LOVO-EVADR细胞组的增殖和迁移能力明显提高(P<0.05)。同时,上皮标志物E-cadherin表达明显降低,而Snail、Slug、ZEB1和ZEB2间质化标志物的表达升高。结论过表达lncRNA EVADR具有促进结直肠癌HCT116和LOVO细胞的增殖与迁移能力,可能通过调节结直肠癌细胞上皮间质转化(EMT)发挥作用。     

靶向干扰前列腺源性ETS因子促进HT29细胞的增殖与侵袭

目的:结直肠癌是常见的消化道肿瘤之一,研究发现在结直肠组织,前列腺源性ETS因子(Prostate-derived Ets factor,PDEF)的表达可以促进分泌性祖细胞向杯状细胞分化,因此结直肠癌的发生可能与PDEF的表达有关。本研究旨在探讨靶向干扰前列腺源性ETS因子对结直肠癌细胞株HT29增殖与侵袭的影响。方法:阳离子脂质体法将PDEF干扰质粒和空白对照空质粒瞬时转染HT29细胞,通过荧光显微镜、RT-PCR、Western blot技术测定正常对照组、空白对照组和shRNA组中PDEF mRNA和蛋白的表达情况;MTT法检测HT29细胞的增殖情况;采用Transwell迁移实验观察细胞侵袭能力。结果:干扰质粒、空质粒成功转染HT29细胞,通过荧光显微镜可以观察到绿色荧光蛋白的表达;Western blot结果可见shRNA组PDEF蛋白的表达较正常对照组和空白对照组降低;MTT法检测发现干扰PDEF基因的表达能够明显促进HT29细胞的增殖(P<0.05);48 h后,shRNA组细胞侵袭能力明显强于正常对照组和空白对照组(P<0.05)。结论:在HT29细胞中干扰PDEF的表达,可以促进细胞的增殖与侵袭。     

周期蛋白E促进结直肠癌SW1116细胞增殖和侵袭

目的 探究周期蛋白E高表达对结直肠癌SW1116细胞增殖和侵袭的影响。方法 将SW116细胞分为周期蛋白E-过表达组、对照组与空载体组，免疫组化法检测各组细胞周期蛋白E的表达；实时定量PCR法检测周期蛋白E mRNA的表达；四甲基偶氮唑盐实验法(MTT)观察细胞增殖能力；流式细胞仪检测细胞周期；Transwell实验检测细胞侵袭能力。结果 与对照组与空载体组相比，周期蛋白E过表达组SW116细胞的周期蛋白E mRNA表达明显升高；在24h和48h时的细胞存活率明显升高；G₀/G₁期细胞比例明显升高，G₂/M期细胞比例明显降低；穿膜细胞数明显增加。结论 周期蛋白E促进结直肠癌SW1116细胞的增殖与侵袭。     

CircRNA锌指RNA结合蛋白在恶性肿瘤中作用研究进展

环状RNA是一类具有特殊共价闭合环状结构的RNA分子,环状RNA锌指核糖核酸结合蛋白(circRNA-ZFR)在诸多恶性肿瘤中呈异常表达,并且其表达水平与肿瘤临床分期、癌细胞转移及患者预后密切相关;circRNA-ZFR可通过内源竞争性吸附miRNA、调节细胞周期、激活多种信号通路等机制参与调控肿瘤的发生发展。深入研究circRNA-ZFR在恶性肿瘤中的表达及作用机制有助于相关肿瘤的早期诊断、靶向治疗和患者预后评估。     

干扰IGF2BP2下调MYC表达抑制结直肠癌细胞增殖、迁移并促进肿瘤免疫

目的 探究胰岛素样生长因子2 mRNA结合蛋白2(IGF2BP2)对结直肠癌细胞增殖、迁移能力和肿瘤免疫微环境的影响及其可能的分子机制。方法 使用癌症基因图谱(TCGA)数据库分析结直肠癌及癌旁组织的IGF2BP2和MYC表达水平。采用RNA干扰技术(RNAi)沉默HCT-116和SW480人结直肠癌细胞的IGF2BP2表达，实时定量PCR检测沉默效果。敲低IGF2BP2后，集落形成实验、 CCK-8实验、 5-乙炔基-2′-脱氧尿苷(EdU)实验检测细胞集落形成和增殖能力，Transwell^TM实验检测细胞迁移能力，实时定量PCR检测IGF2BP2、 MYC、肿瘤坏死因子α(TNF-α)、转化生长因子β(TGF-β)、白细胞介素10(IL-10)的mRNA表达。Western blot法测定IGF2BP2、 MYC的蛋白表达，RNA免疫共沉淀后实时定量PCR(RIP-qPCR)检测HCT-116细胞中IGF2BP2与MYC mRNA结合能力。结果 TCGA数据库结果表明，IGF2BP2和MYC在结直肠癌组织中的表达显著高于癌旁组织，且IGF2BP2高表达的结直肠...     

AngⅡ促进大鼠血管平滑肌细胞增殖和迁移

血管平滑肌细胞(vascular smooth muscle cells,VSMCs)的增殖、迁移和细胞外基质的合成是高血压、动脉粥样硬化和血管成形术后再狭窄等血管重塑性疾病发生、发展的重要细胞病理学基础[1].血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)的促生长作用参与了高血压、动脉粥样硬化、血管再狭窄等血管增殖性疾病的发生和发展.本实验观察AngⅡ对VSMCs细胞增殖及迁移的影响,进一步阐明血管增殖性疾病的发病机理,为临床防治提供理论依据.1材料与方法1.1细胞培养与试剂:80～100 g健康雄性SD大鼠,取胸腹主动脉血管中膜用贴块法分离、培养VSMCs[2].取3～6代细胞进行实验.待细胞生长至70％～80％汇合后换用无血清培养液饥饿培养16 h,使细胞处于静止期,然后换用含2％FBS的培养液,分别加入不同浓度(10-8、10-7和10-6 mol/L)的AngⅡ(Sigma公司)孵育24h,或10-7 mol/L的AngⅡ孵育不同时间(3、6、12、24和48 h),收集细胞用于实验.     

pH regulation in HT29 colon carcinoma cells

The pH regulation in HT₂₉ colon carcinoma cells has been investigated using the pH-sensitive fluorescent indicator 2,7-biscarboxyethyl-5(6)-carboxyfluorescein (BCECF). Under control conditions, intracellular pH (pH_i) was 7.21±0.07 (n=22) in HCO ₃ ^– -containing and 7.21±0.09 (n=12) in HCO ₃ ^– -free solution. HOE-694 (10 mol/l), a potent inhibitor of the Na⁺/H⁺ exchanger, did not affect control pH_i. As a means to acidify cells we used the NH ₄ ⁺ /NH₃ (20 mmol/l) prepulse technique. The mean peak acidification was 0.37±0.07 pH units (n=6). In HCC ₃ ^– -free solutions recovery from acid load was completely blocked by HOE-694 (1 mol/l), whereas in HCO3 ₃ ^– -containing solutions a combination of HOE-694 and 4,4-diisothiocyanatostilbene-2, 2-disulphonate (DIDS, 0.5 mmol/l) was necessary to show the same effect. Recovery from acid load was Na⁺-dependent in HCO ₃ ^– -containing and HCO ₃ ^– -free solutions. Removal of external Cl^– caused a rapid, DIDS-blockable alkalinization of 0.33±0.03 pH units (n=15) and of 0.20±0.006 pH units (n=5), when external Na⁺ was removed together with Cl^–. This alkalinization was faster in HCO ₃ ^– -containing than in HCO ₃ ^– -free solutions. The present observations demonstrate three distinct mechanisms of pH regulation in HT₂₉ cells: (a) a Na⁺/H⁺ exchanger, (b) a HCO ₃ ^– /Cl^– exchanger and (c) a Na⁺-dependent HCC ₃ ^– transporter, probably the Na⁺-HCO ₃ ^– /Cl^– antiporter. Under HCO ₃ ^– — free conditions the Na⁺/H⁺ exchanger fully accounts for recovery from acid load, whereas in HCO ₃ ^– -containing solutions this is accomplished by the Na⁺/H⁺ exchanger and a Na⁺-dependent mechanism, which imports HCO ₃ ^– . Recovery from alkaline load is caused by the HCO ₃ ^– /Cl^– exchanger.This study was supported by DFG Gr 480/10     

Small and intermediate conductance chloride channels in HT29 cells

Recently, it has been shown that intermediate conductance outwardly rectifying chloride channels (ICOR) are blocked by cytosolic inhibitor (C. I.) found in the cytosol of human placenta and epithelial cells. C. I. also reduced the baseline current in excised membrane patches of HT₂₉ cells. In the present study, this effect of C. I. was characterized further. Heat treated human placental cytosol was extracted in organic solvents and dissolved in different electrolyte solutions. It is shown that the reduction of baseline conductance (g _o) is caused by inhibition of small non-resolvable channels, which are impermeable to Na⁺ and SO₄ ^2–, but permeable to Cl^–. The regulation of these small Cl^–-conducting channels (g _o) and of ICOR was examined further. First, no activating effects of protein kinase A (PKA) on the open probability (P _o) of the ICOR or on the g_o) were observed. The P_o of the ICOR was reduced by 22% in a Ca²⁺-free solution. g _o was insensitive to changes in the Ca²⁺ activity. The effects of C. I. from a cystic fibrosis (CF) placenta and the CF pancreatic duct cell line CFPAC-1 were compared with the effects of corresponding control cytosols, and no significant differences between CF and control cytosols were found. We conclude that the excised patches of HT₂₉ cells contain ICOR and small non-resolvable Cl^–-conducting channels which are similarly inhibited by C. I. Apart from a weak effect of Ca²⁺ on the ICOR, g _o and the ICOR do not seem to be directly controlled by Ca²⁺ or PKA. C. I. of normal and CF epithelia have a similar inhibitory potency on Cl^– channels.     

Transmitter-induced changes of the membrane voltage of HT29 cells

The colonic carcinoma cell line HT₂₉ was used to examine the influence of agonists increasing cytosolic cAMP and Ca²⁺ activity on the conductances and the cell membrane voltage (V _m). HT₂₉ cells were grown on glass cover-slips. Cells were impaled by microelectrodes 4–10 days after seeding, when they had formed large plaques. In 181 impalements V _m was –51±1 mV. An increase in bath K⁺ concentration from 3.6 mmol/l to 18.6 mmol/l or 0.5 mmol/l Ba²⁺ depolarized the cells by 10±1 mV (n=49) or by 9±2 mV (n=3), respectively. A decrease of bath Cl^– concentration from 145 to 30 mmol/l depolarized the cells by 11±1 mV (n=24). Agents increasing intracellular cAMP such as isobutylmethylxanthine (0.1 mmol/l), forskolin (10 mol/l) or isoprenaline (10 mol/l) depolarized the cells by 6±1 (n=13), 15±3 (n=5) and 6±2 (n=3) mV, respectively. In hypoosmolar solutions (225 mosmol/l) cells depolarized by 9±1 mV (n=6). Purine and pyrimidine nucleotides depolarized the cells dose-dependently with the following potency sequence: UTP > ATP > ITP > GTP > TIP > CTP = 0. The depolarization by ATP was stronger than that by ADP and adenosine. The muscarinic agonist carbachol led to a sustained depolarization by 27±6 mV (n=5) at 0.1 mmol/l, and to a transient depolarization by 12±4 mV (n=5) at 10 mol/l. Neurotensin depolarized with a half-maximal effect at around 5 nmol/l. The depolarization induced by nucleotides and neurotensin was transient and followed by a hyperpolarization. We confirm that HT₂₉ cells possess Cl^–- and K⁺-conductive pathways. The Cl^– conductance is regulated by intracellular cAMP level, cytosolic Ca²⁺ activity, and cell swelling. The K⁺ conductance in HT₂₉ cells is regulated by intracellular Ca²⁺ activity.Supported by DFG Gre 480/10 and GIF Proj. no. I-86-100.10/ 88     

Agonist-induced intracellular Ca2+ transients in HT29 cells

In the present study we have investigated the mechanism of intracellular Ca²⁺ activity ([Ca²⁺]_i) changes in HT₂₉ cells induced by adenosine triphosphate (ATP), carbachol (CCH), and neurotensin (NT). [Ca²⁺]_i was measured with the fluorescent Ca²⁺ indicator fura-2 at the single-cell level or in small cell plaques with high time resolution (1–40Hz). ATP and CCH induced not only a dose-dependent [Ca²⁺]_i peak response, but also changes of the plateau phase. The [Ca²⁺]_i plateau was inversely dependent on the ATP concentration, whereas the CCH-induced [Ca²⁺]_i plateau increased at higher CCH concentrations. NT showed (from 10^–10 to 10^–7 mol/l) in most cases only a [Ca²⁺]_i spike lasting 2–3 min. The [Ca²⁺]_i plateau induced by ATP (10^–6 mol/l) and CCH (10^–5 mol/l) was abolished by reducing the Ca²⁺ activity in the bath from 10^–3 to 10^–4 mol/l (n=7). In Ca²⁺-free bathing solution the [Ca²⁺]_i peak value for all three agonists was not altered. Using fura-2 quenching by Mn²⁺ as an indicator of Ca²⁺ influx the [Ca²⁺]_i peak was always reached before Mn²⁺ influx started. Every agonist showed this delayed stimulation of the Ca²⁺ influx with a lag time of 23±1.5 s (n=15) indicating a similar mechanism in each case. Verapamil (10^–6–10^–4 mol/l) blocked dose dependently both phases (peak and plateau) of the CCH-induced [Ca²⁺]_i increase. Short pre-incubation with verapamil augmented the effect on the [Ca²⁺]_i peak, whereas no further influence on the plateau was observed. Ni²⁺ (10^–3 mol/l) reduced the plateau value by 70%.     

生长因子受体结合蛋白-2抑制肠癌细胞HT29增殖

目的 研究Grb2 shRNA转染对肠癌细胞HT29增殖相关信号通路的影响,探讨以Grb2为肠癌治疗靶点的可行性.方法 应用shRNA慢病毒质粒系统,将Grb2 shRNA转染至293T细胞,获得5株不同序列Grb2 shRNA慢病毒颗粒,并感染肠癌HT29细胞,分别获得的5株感染Grb2 shRNA慢病毒颗粒的肠癌HT29细胞系为实验组(即感染Grb2 shRNA的细胞HT29/shGrb2-69、HT29/shGrb2-70、HT29/shGrb2-71、HT29/shGrb2-72、HT29/shGrb2-73),以eGFP shRNA慢病毒感染肠癌HT29细胞为阴性对照组.MTT法检测细胞增殖情况,RT-PCR检测Grb2 mRNA表达,Western blot检测Grb2、P42/44 ERK、磷酸化P42/44 ERK、Akt、磷酸化Akt(P-Akt)和STAT5等信号通路分子表达的改变.结果 感染shGrb2病毒72 h,HT29/shGrb2-69、HT29/shGrb2-73两株细胞在mRNA和蛋白水平均出现抑制现象.HT29/shGrb2-69、HT29/shGrb2-73细胞在感染后24h A值分别为0.176±0.045,0.186±0.013,感染48 h后为0.347±0.048、0.382±0.041均显著高于空白对照、阴性对照(P ＜0.001),72 h为0.934±0.038、0.983±0.205高于空白对照、阴性对照(P＜0.01);感染后72 h,phospho-P42/44 ERK、Akt、phospho-Akt明显下降,而ERK、STAT5表达不受影响.结论 在HT29细胞,Grb2 mRNA和蛋白水平上明显抑制,可诱导HT29细胞增殖和相关信号传导通路分子表达下调.     

构建hTNF-α/293基因细胞对人结肠癌细胞增殖影响的实验研究

目的通过体外实验研究观察稳定转染hTNF—α／293基因细胞对人结肠癌（LOVO）细胞生长增殖影响。方法采用RT—PCR和ELISA检测稳定转染hTNF-α／293基因细胞和Hek-293细胞mRNA和蛋白表达水平。观察体外培养中,hTNF—α／293基因细胞与LOVO细胞共同培养,于不同的时间点,采用噻唑蓝MTF法检测LOVO肿瘤细胞增殖的活性。结果重组质粒转染Hek。293细胞后,Western blot检测到了hTNF-α蛋白体外表达,检测表明hTNFα／293细胞组和hTNFα阳性组对共培养的LOVO细胞的增殖具有明显的抑制作用,且具有良好的量效关系。结论提示稳定转染hTNF—α/293对LOVO细胞增殖有明显抑制效应,且呈现出良好的数量依赖关系。由于TNF—α／293基因细胞可有效分泌hTNFα蛋白,并能分泌到细胞外。     

Induction of oxidative DNA damage by Helicobacter pylori in HT29 cells

Infection with Helicobacter pylori has been associated with the development of gastric adenocarcinoma in humans. Several routes have been implicated, the main one being oxidative DNA damage resulting from chronic inflammation, which accompanies infection. However, DNA has been demonstrated in human cells after in vitro incubation with H. pylori sonicates. Using the fragment length analysis using restriction enzymes (FLARE) assay, this study investigates the DNA damaging potential of three clinical isolates of H. pylori on cultured HT29 cells. Significant amounts of oxidative DNA damage were detected in HT29 cells following a 72-hour incubation with each H. pylori isolate. As tumour induction is a known consequence of oxidative DNA damage, chronic infection with the organism may lead to the development of adenocarcinoma of the stomach.     

重组新城疫病毒IL29抑制人胃癌细胞系BGC的增殖与迁移

目的探讨表达IL-29的重组新城疫病毒Lo Sota株(rL-IL29)对人胃癌BGC细胞增殖及迁移的影响及其机制。方法将体外培养的人胃癌BGC细胞分为对照组、rL-IL29组和Lo Sota株新城疫病毒(NDV)组,分别经PBS、rL-IL29及NDV感染处理后进行下一步实验。蛋白质印迹检测BGC细胞中IL-29、NDV、P-ERK、MMP2、p-AKT蛋白的表达;CCK8法、划痕试验及Transwell小室法侵袭实验检测胃癌BGC细胞的增殖、迁移能力。结果IL-29蛋白仅在rL-IL29组表达,NDV蛋白在IL-29组及NDV组均稳定表达,且明显高于PBS组(P<0.05);rL-IL29感染BGC细胞后BGC细胞的增殖及迁移能力明显减弱,且rL-IL29的抑制较NDV组作用更强;BGC细胞经rL-IL29感染后P-ERK、MMP2(66 ku/72 ku)、p-AKT蛋白表达较对照组及NDV组明显减弱(P<0.05)。结论rL-IL29抑制胃癌BGC细胞的增殖、侵袭及迁移可能与ERK,AKT等信号通路相关。     

肝细胞生长因子基因转染对人脐静脉内皮细胞增殖、迁移的影响

目的:观察HGF基因对人脐静脉内皮细胞增殖、迁移的影响。方法:从已有质粒pRc/CMV-HGF中扩增出HGF基因,将其克隆到含增强型绿色荧光蛋白的真核表达载体中,构建重组质粒pEGFP-HGF,酶切及测序鉴定正确后,用脂质体将重组质粒pEGFP-HGF转染到人脐静脉细胞株ECV304中,G418筛选获得稳定表达细胞克隆,采用荧光显微镜观察、RT-PCR、免疫细胞化学方法检测鉴定重组质粒的表达情况;酶联免疫吸附法(ELISA)检测稳定表达细胞中HGF的含量;再以MTT法检测转染重组质粒后细胞增殖的改变,Transwell Migration实验检测细胞迁移能力的改变。结果:所构建重组质粒经酶切图谱分析和序列测定证实构建成功;荧光显微镜下观察到有绿色荧光;RT-PCR证实HGFmRNA在转染阳性细胞高表达;免疫细胞化学证实转染pEGFP-HGF质粒的细胞有HGF蛋白的表达;ELISA检测细胞培养基中HGF含量可达112.3 ng/ml,MTT法、TranswellMigration测定转染pEGFP-HGF阳性细胞的增殖、迁移能力明显高于对照组(P<0.01)。结论:重组质粒pEGFP-HGF能够在内皮细胞株ECV304转录、表达;表达的活性蛋白HGF刺激ECV304的增殖、迁移,为进一步应用于基因治疗奠定实验基础。     

Survivin基因对大肠癌细胞HT29生物学行为的影响

目的探讨Survivin基因对人大肠癌细胞HT29增殖及凋亡的影响。方法以脂质体Lip-2000为载体,用针对Survivin特异靶点的siRNA转染人大肠癌细胞HT29后,应用免疫细胞化学SP法、Western blot技术检测Survivin蛋白表达变化;采用MTT法检测细胞增殖;采用流式细胞技术检测细胞凋亡。结果免疫细胞化学结果:正常对照组、脂质体对照组及阴性错配对照组中Survivin均呈细胞质强阳性表达,Survivin-siRNA组细胞质呈弱阳性表达;Western blot检测结果:Survivin-siRNA组细胞的蛋白条带亮度明显低于正常对照组、脂质体对照组和阴性错配对照组;MTT检测结果:与阴性错配对照组相比,Survivin-siRNA组细胞生长出现明显的抑制(P<0.05)。不同时段(24、48、72 h)肿瘤细胞增殖抑制率之间差异有显著性(P<0.05);流式细胞术检测结果显示Survivin-siRNA组细胞凋亡比例显著高于空白对照组及阴性错配对照组(P<0.01)。结论 Sur-vivin基因参与调控大肠癌细胞的增殖和凋亡,Survivin有望成为大肠癌基因治疗的新靶点。