沉默激酶功能区受体抑制前列腺癌PC-3细胞的裸鼠体内成瘤能力

目的 研究激酶功能区受体(KDR)基因表达沉默后对前列腺癌PC-3细胞裸鼠体内成瘤能力的影响.方法 将15只5周龄BALB/c雄性裸鼠随机分为干扰组、阴性质粒组和未转染组,每组5只.分别接种构建的pSilencer 3.1-KDR siRNA表达质粒转染PC-3细胞、阴性对照质粒pSilencer3.1-NC转染PC-3细胞以及未转染的PC-3细胞于裸鼠皮下;观察各组PC-3细胞在裸鼠体内成瘤率、瘤体生长速度以及平均瘤质量等方面的变化,RT-PCR和Western blot技术检测瘤体KDR基因和蛋白表达.结果 pSilencer3.1KDR质粒转染组的裸鼠瘤体生长速度明显慢于未转染组和pSilencer3.1-NC质粒转染组;与未转染组和PSilencer3.1-NC组相比,pSilencer3.1-KDR组肿瘤的生长受到明显抑制,平均体积较小(0.28 cm3 vs 0.721 cm3,0.715 cm3,P＜0.01),平均瘤质量较轻(0.14g vs 0.648g,0.635g,P＜0.01);裸鼠肿瘤组织中KDR mRNA和蛋白的表达明显降低.结论 RNAi介导的KDR基因沉默可显著影响PC-3细胞裸鼠体内的瘤体生长速度,KDR有可能成为肿瘤治疗的新靶点.     

人胃癌转移鼠模型的构建及移植瘤的阶段性研究

目的：建立人胃癌的“转移鼠”模型,为研究胃癌转移打下基础。方法：将人胃低分化粘液腺癌ＭＧＣ－８０３细胞悬液先在裸小鼠皮下接种成瘤,再取瘤组织块分别接种到裸鼠的皮下、胃壁上（转移鼠模型）,分早（〈２０天）、中（２０～４０天）、晚（〉４０天）,４个阶段观察移植瘤的生长侵袭转移情况。结果：皮下组移植成瘤率为８２．１％（２３／２８）,早、中阶段未见转移,晚期肺转移率５７．１％（４／７）。胃壁组移植成瘤率为     

荧光标记肿瘤转移体内模型的建立

目的 建立一种带荧光标记的肿瘤转移模型并探讨其应用价值.方法 人胃癌MGC-803细胞和小鼠宫颈癌U14细胞进行体外传代培养,转染pEGFP-N1质粒,24h检测转染效率,用无限稀释法筛选稳定表达绿色荧光蛋白(GFP)的单克隆细胞株MGC-803-GFP和U14-GFP.分别体内移植于BALB/c-nn裸鼠和C57BL/6J小鼠,观察成瘤潜伏期,绘制体内生长曲线,利用活体荧光成像系统活体连续观察GFP在体内的表达,观察肺部和淋巴结的转移情况,计算转移率.免疫组织化学检测与转移相关的分子CD44和E-cadherin在移植瘤中的表达.结果 MGC-803细胞和U14细胞pEGFP-N1转染24 h后的转染效率分别为30%和60%.获得了GFP(+)的单克隆MGC-803-GFP细胞株和U14-GFP细胞株.MGC-803-GFP在BALB/c-nu裸鼠和U14-GFP在C57BL/6J小鼠移植成瘤的潜伏期分别是3～5 d和2～4 d,成瘤率均为100%.利用活体荧光成像系统连续观察,可以清楚直观地观察表达GFP的MGC-803-GFP移植瘤在体内的生长,接种后第60天处死全部荷瘤鼠,解剖后仅有1只可见同侧腋窝下淋巴结的转移.接种U14-GFP后,分别在第28、37和52天观察了荷瘤小鼠肿瘤转移的发展过程.在U14-GFP原发瘤体积达到≥5 cm3时,肺部和淋巴结转移率分别为67%和100%.在MGC-803-GFP和U14-GFP的移植瘤中都可以检测到CD44的表达,而无E-cadherin的表达.结论 成功建立了表达绿色荧光蛋白单克隆细胞株MGC-803-GFP和U14-GFP,体内移植建立了荧光标记的肿瘤转移模型.该模型可用于可视化肿瘤体内的研究.     

食管癌耐药皮下移植瘤裸鼠模型建立

 [摘要] 目的 建立食管癌耐药裸鼠模型及探讨食管癌耐药机制。方法 4周龄的BALB/c nu/nu裸小鼠36只随机分组分为6组,每组6只,左前肢肩胛下皮下分别接种食管癌细胞Eca109及食管癌耐药细胞Eca109/ABCG2,建立裸鼠皮下移植瘤模型。成瘤后腹腔注射阿霉素（Adriamycin, ADM）,1、4mg/kg,1次/3d 共注射7次,空白对照组使用生理盐水(normal saline, NS)代替ADM。RT-PCR方法检测移植瘤细胞中三磷酸腺苷结合转运蛋白G2（ATP-binding cassette transporter G2,ABCG2）mRNA 表达情况,流式细胞术(Flow cytometry, FCM)检测移植瘤细胞中ABCG2蛋白、凋亡及细胞中ADM含量。结果 成功建立裸鼠食管癌耐药细胞移植瘤模型,皮下接种细胞一周后成瘤,成瘤率100%。实验结束后,注射ADM药物的裸鼠,接种Eca109/ABCG2细胞的皮下移植瘤体积、重量和ABCG2 mRNA、蛋白表达量显著高于接种Eca109细胞移植瘤（P<0.05）,但细胞凋亡率及细胞内ADM含量显著降低（P<0.05）。结论 接种Eca109/ABCG2细胞的裸鼠皮下移植瘤模型是较好的食管癌耐药动物模型,具有ABCG2耐药表型,为研究ABCG2与食管癌耐药关系提供了较理想的动物模型。     

人乳头瘤病毒阴性的喉鳞癌细胞系的建立

目的 建立1株人乳头状瘤病毒（HPV）阴性的喉鳞状细胞癌细胞系,为体外研究喉癌提供理想的实验模型。方法 以逆转录聚合酶链反应（RT-PCR）证实为HPV阴性的高分化喉鳞癌手术切除标本接种于裸鼠皮下,取连续传代2次的裸鼠皮下移植瘤进行体外原代培养。通过光镜、电镜、生长曲线、细胞周期时相、软琼脂克隆实验、异种移植成瘤实验、角蛋白、癌胚抗原及HPV检测,对其生物学特性进行初步分析。结果 经裸鼠过渡所建立的高分化喉鳞癌细胞系（Lscc-02）目前已传至86代,细胞生长增殖稳定。该细胞系呈单层形式生长,群体倍增时间为39．1h。透射电镜下见胞质内典型的张力原纤维,细胞问以桥粒方式连接。染色体为人类核型,呈亚三倍体,众数分布在63～72。该细胞系具有恶性肿瘤细胞生长特征：软琼脂中形成克隆,裸鼠接种成瘤且形态结构、分化程度与原发瘤相似。免疫组织化学显示高分子量细胞角蛋白及癌胚抗原阳性,PCR显示HPV阴性。结论 建立Lscc-02细胞系为研究无HPV感染喉癌的发生、发展规律及HPV与喉癌演进的关系提供了有价值的体外模型。     

新发现1例人卵巢上皮癌组织移植裸鼠形成的“端着丝粒染色体”恶性细胞系

目的 按照常用肿瘤细胞建系方法,以人卵巢上皮癌组织移植免疫缺陷小鼠,通过原代培养建立永生化细胞系,为人体肿瘤的研究提供体外研究模型。 方法 将1例卵巢浆液性乳头状癌IIIcG3患者手术切除的肿瘤组织接种裸鼠皮下成瘤,通过体外原代培养,建立1株悬浮生长的细胞系。通过光学显微镜、电子显微镜、生长曲线测定、染色体分析、克隆形成实验、双层软琼脂培养、裸鼠接种等,对其生物学特性进行研究。 结果 该细胞系已传至100代以上,命名为WSZ。其生物学特性为：形态学观察细胞呈悬浮球形生长状态;细胞生长增殖旺盛,对数期细胞群体倍增时间约15.8h;染色体为16~135条,以68和69条染色体为多见,染色体分析显示,基本全部为端着丝粒染色体;细胞克隆形成率为89.3%,具有软琼脂集落形成能力;异种移植实验表明10⁶细胞在裸鼠皮下可成瘤, 而100个细胞接种非肥胖型糖尿病/重症联合免疫缺陷（NOD/SCID）小鼠即可形成皮下肿瘤。 结论 WSZ能够在体外长期生长和稳定传代,WSZ是一高度恶性的细胞系。     

p75NGFR对胰腺癌细胞株SW1990生物学行为的影响

目的通过体内和体外实验,探讨p75NGFR在胰腺癌SW1990细胞生长、分化以及侵袭中的作用。方法采用脂质体转染法将含p75NGFR的真核表达质粒转染人胰腺癌细胞株SW1990,建立稳定表达p75NGFR的细胞模型;应用MTT法、平板克隆形成实验以及流式细胞技术分别检测细胞的生长曲线、克隆形成能力以及细胞周期变化;建立胰腺癌的裸鼠皮下移植瘤和胰腺原位移植瘤模型,观察p75NGFR对SW1990细胞裸鼠成瘤能力、肿瘤组织学分化、细胞侵袭和转移的影响。结果与对照组相比较,转染p75NGFR的SW1990细胞其生长速度缓慢（P〈0.01）,克隆形成能力降低（P〈0.05）;转染细胞的细胞周期改变表现为G1期细胞明显增多和S期细胞明显减少（均为P〈0.01）。与对照组相比较,转染组裸鼠皮下以及胰腺原位的成瘤率以及肿瘤体积减小（P〈0.01）,肿瘤的生长缓慢,组织学分化差,浸润性生长趋势不明显,未见肿瘤卫星现象。结论体外实验均发现p75NGFR通过阻滞细胞周期进程而显著抑制胰腺癌细胞株的生长,体内研究发现p75NGFR可抑制裸鼠皮下及胰腺原位移植瘤的形成、分化和侵袭,提示p75NGFR与胰腺癌的生物学行为密切相关。     

PC-1基因表达诱导NIH3T3细胞恶性转化

目的 通过建立稳定表达外源PC-1基因的小鼠成纤维细胞株,初步探讨PC-1基因表达对肿瘤发生、发展的影响。方法 通过脂质体介导的方法,将真核表达载体pcDNA3、1(-)／myc-his-pc-1稳定转染NIH3T3细胞,之后利用PCR、逆转录PCR(RT-PCR)技术,确定外源PC-1基因在靶细胞染色体上的整合及在转录水平的表达。通过细胞形态学分析、MTT实验、细胞周期分析、软琼脂集落形成和裸鼠成瘤实验,观察PC-1基因表达对NIH3T3生物学特性的影响。结果建立了稳定转染PC-1基因的NIH3T3细胞株。PC-1基因表达的小鼠成纤维细胞NIH3T3生长速度加快,在软琼脂上生长并形成集落,接种裸鼠后可成瘤(6／6)。结论 PC-1基因在NIH3T3细胞中稳定表达具有诱导正常NIH3T3细胞发生恶性转化的重要生物功能。     

逆转录病毒介导IL-27基因对胰腺癌细胞在裸鼠体内的成瘤抑制作用及其机制

目的:探讨IL-27基因在人胰腺癌Aspc1细胞中的抗肿瘤作用及免疫机制。方法:以逆转录病毒为载体,采用基因转染的方法用G418梯度筛选法建立转染IL-27基因的Aspc1细胞,用RT-PCR检测其基因导入,ELISA法检测IL-27的分泌。将Aspc1/IL-27、Aspc1/LXSN和Aspc1细胞接种于裸鼠皮下,观察成瘤性、移植瘤的生长情况。10天时取3组裸鼠脾脏,用ELISA法检测3组小鼠脾细胞在Aspc1诱导下IFN-γ、TNF-α和IL-12的产生情况,乳酸脱氢酶法检测脾细胞杀伤活性。结果:成功建立稳定转染的Aspc1/IL-27细胞株,ELISA检测Aspc1/IL-27细胞培养上清中IL-27的分泌量为(121.56±6.29)pg/ml,而在Aspc1/LXSN细胞和Aspc1细胞的培养上清中未检出IL-27。IL-27基因转染组裸鼠皮下结节生长速度明显慢于接种空载体转染组及未转染组;接种Aspc1/IL-27细胞的裸鼠脾细胞可产生较水平的IFN-γ、TNF-α和IL-12等细胞因子,与接种Aspc1/LXSN细胞和Aspc1细胞组裸鼠的脾细胞相比明显增高(P0.01),接种Aspc1/IL-27细胞的裸鼠脾细胞杀伤活性显著性升高(P0.01)。结论:转染IL-27基因的裸鼠胰腺癌细胞所分泌的IL-27具有生物学活性,通过增强细胞免疫功能在裸鼠体内发挥抗肿瘤作用。     

人绒毛膜癌裸鼠原位移植模型的建立

目的建立人绒毛膜癌裸鼠原位移植瘤模型。方法培养人绒毛膜癌细胞系JAR,制备JAR单细胞悬液,给5只8周龄BALB/c裸鼠经皮下注射建立皮下移植瘤模型。待裸鼠皮下成瘤后,无菌条件下取瘤组织并切成1 mm^3组织块,通过手术方式植入10只10周龄BALB/c裸鼠子宫腔内,裸鼠濒死状时4%水合氯醛(10 g/kg)腹腔注射麻醉处死,观察子宫成瘤及腹腔转移情况。解剖取子宫原位移植瘤、腹腔内转移瘤、腹腔淋巴结及其他脏器组织标本,通过组织病理学检查进行鉴定。结果10只BALB/c裸鼠中共有7只裸鼠子宫内可见移植瘤肿块形成,其中2只可同时观察到子宫移植瘤和腹膜转移瘤。在病理学形态和结构上,皮下移植瘤模型、原位移植模型和腹膜转移瘤的瘤细胞与人绒毛膜癌细胞系JAR一致。结论成功建立人绒毛膜癌JAR细胞的BALB/c裸鼠原位移植瘤模型。     

Increased metastatic potential in human prostate carcinoma cells by overexpression of arachidonate 12-lipoxygenase

Arachidonate 12-lipoxygenase (LOX) converts arachidonic acid to 12(S)-hydroxyeicosatetraenoic acid (HETE), a bioactive lipid implicated in tumor angiogenesis, growth, and metastasis. Alteration in 12-LOX expression or activity has been reported in various carcinomas including prostate carcinoma. However, little is known about the impact of the altered expression or activity of 12-LOX on tumor metastasis. In the present study, we examined whether or not an increase in 12-LOX expression in human prostate carcinoma cells can modulate their metastatic potential. We report that increased expression of 12-LOX in PC-3 cells caused a significant change in cell adhesiveness, spreading, motility, and invasiveness. Specifically 12-LOX transfected PC-3 cells were more adhesive toward vitronectin, type I and IV collagen, but not to fibronectin or laminin, than cells transfected with control vector. Increased spreading on vitronectin, fibronectin, collagen type I and IV also was observed in 12-LOX transfected PC-3 cells when compared to control PC-3 cells. The increased spreading of 12-LOX transfected PC-3 cells was blocked by treatment with 12-LOX inhibitors, baicalein and CDC. 12-LOX transfected PC-3 cells were more invasive through Matrigel than cells transfected with control vector. In vivo, tumor cell invasion to surrounding muscle or fat tissues was more frequent in nude mice bearing s.c. tumors from 12-LOX transfected PC-3 cells than in those from control vector transfected cells. When injected via the tail vein into SCID mice with implanted human bone fragments, there was an increase in tumor metastasis to human bone by 12-LOX transfected PC-3 cells in comparison to control vector transfected cells. Taken together, our data suggest that an increase in 12-LOX expression enhances the metastatic potential of human prostate cancer cells. This revised version was published online in July 2006 with corrections to the Cover Date.     

Treatment of prostate carcinoma with (galectin-3)-targeted HPMA copolymer-(G3-C12)-5-Fluorouracil conjugates

Galectin-3 (Gal-3), over-expressed on a variety of human tumor cells, is a potential binding site for targeted metastatic prostate cancer therapy. The aim of this study was to develop a G3-C12-mediated drug delivery system based on N-(2-hydroxypropyl) methacrylamide (HPMA) copolymers targeting to Gal-3-expressed human PC-3 prostate carcinoma cells. 5-Fluorouracil (5-Fu), an anti-tumor agent, was selected as a model drug. G3-C12, a binding peptide, which specifically binds to the carbohydrate-recognition domain (CRD) of Gal-3, was attached to HPMA copolymers as a targeting moiety. Compared with non-targeted conjugates (P-Fu), Gal-3-targeted HPMA copolymer-(G3-C12)-5-Fu conjugates (P-(G3-C12)-Fu) displayed a superior intracellular internalization followed by enhanced cytotoxicity and apoptosis-induction. Subsequently, the in vitro migration study on PC-3 cells indicated that P-(G3-C12)-Fu was able to efficiently inhibit the cell migration ability after wounding. On PC-3 tumor-bearing mice model, G3-C12-modified copolymers showed a higher tumor accumulation coupled with a faster clearance from blood circulation than non-modified ones. Finally, Gal-3-targeted conjugates significantly improved the anti-tumor activity of 5-Fu in nude mice bearing PC-3 tumor xenografts. Consequently, G3-C12 would be a promising targeting moiety for cell-specific prostate cancer therapy in future.     

Effect of curcumin on Bcl-2 and Bax expression in nude mice prostate cancer

Prostate cancer is a common malignant tumor in urinary system. Curcumin has curative effect on many kinds of cancers and can inhibit prostate cancer (PC)-3 cells proliferation. This study aimed to explore the curcumin induced prostate cancer cell apoptosis and apoptosis related proteins Bcl-2 and Bax expression. PC-3 cells were injected subcutaneously to the nude mice to establish the tumor model. The nude mice were randomly divided into group C (normal saline), group B (6% polyethylene glycol and 6% anhydrous ethanol), group H, M, L (100 mg/kg, 50 mg/kg, and 25 mg/kg curcumin). The tumor volume was measured every 6 days to draw the tumor growth curve. The mice were killed at the 30^th day after injection to weight the tumor. TUNEL assay was applied to determine cell apoptosis. Immunohistochemistry was used to detect Bcl-2 and Bax expression. The tumor volume and weight in group H, M, L were significantly lower than the control group (C, B) (P<0.05), and the inhibitory rate increased following the curcumin dose increase. Compared with the control group, Bcl-2 expression in group H, M, L gradually decreased, while Bax protein expression increased (P<0.05). The cell apoptosis rate showed no statistical difference between group B and C, while it increased in curcumin group H, M, and L (P<0.05). Curcumin could inhibit PC-3 growth, decrease tumor volume, reduce tumor weight, and induce cell apoptosis under the skin of nude mice by up-regulating Bax and down-regulating Bcl-2.     

In vivo monitoring of tumor relapse and metastasis using bioluminescent PC-3M-luc-C6 cells in murine models of human prostate cancer

We used the bioluminescent human prostate carcinoma cell line PC-3M-luc-C6 to non-invasively monitor in vivo growth and response of tumors and metastasis before, during and after treatments. Our goal was to determine the utility of a luciferase-based prostate cancer animal model to specifically assess tumor and metastatic recurrence in vivo following chemotherapy. Bioluminescent PC-3M-luc-C6 cells, constitutively expressing luciferase, were implanted into the prostate or under the skin of mice for primary tumor assessment. Cells were also injected into the left ventricle of the heart as an experimental metastasis model. Weekly serial in vivo images were taken of anesthetized mice that were untreated or treated with 5-fluorouracil or mitomycin C. Ex vivo imaging and/or histology was used to confirm and localize metastatic lesions in various tissues initially detected by images in vivo. Our in vivo data detected and quantified early inhibition of subcutaneous and orthotopic prostate tumors in mice as well as significant tumor regrowth post-treatment. Local and distal metastasis was observed within seven days following intracardiac injection of PC-3M-luc-C6 cells. Differential drug responses and metastatic tumor relapse patterns were distinguished over time by in vivo imaging depending on the metastatic site. The longitudinal evaluation of bioluminescent tumor and metastatic development within the same cohorts of animals permitted sensitive and quantitative assessment of both primary and metastatic prostate tumor response and recurrence in vivo.     

King Cobra (Ophiophagus hannah) Venom L-Amino Acid Oxidase Induces Apoptosis in PC-3 Cells and Suppresses PC-3 Solid Tumor Growth in a Tumor Xenograft Mouse Model

King cobra (Ophiophagus hannah) venom L-amino acid oxidase (OH-LAAO), a heat stable enzyme, has been shown to exhibit very potent anti-proliferative activity against human breast and lung tumorigenic cells but not in their non-tumorigenic counterparts. We further examine its in vitro and in vivo anti-tumor activity in a human prostate adenocarcinoma (PC-3) model. OH-LAAO demonstrated potent cytotoxicity against PC-3 cells with IC₅₀ of 0.05 µg/mL after 72 h incubation in vitro. It induced apoptosis as evidenced with an increase in caspase-3/7 cleavages and an increase in annexin V-stained cells. To examine its in vivo anti-tumor activity, we treated PC-3 tumor xenograft implanted subcutaneously in immunodeficient NU/NU (nude) mice with 1 µg/g OH-LAAO given intraperitoneally (i.p.). After 8 weeks of treatment, OH-LAAO treated PC-3 tumors were markedly inhibited, when compared to the control group (P <0.05). TUNEL staining analysis on the tumor sections showed a significantly increase of apoptotic cells in the LAAO-treated animals. Histological examinations of the vital organs in these two groups showed no significant differences with normal tissues, indicating no obvious tissue damage. The treatment also did not cause any significant changes on the body weight of the mice during the duration of the study. These observations suggest that OH-LAAO cytotoxic effects may be specific to tumor xenografts and less to normal organs. Given its potent anti-tumor activities shown in vitro as well as in vivo, the king cobra venom LAAO can potentially be developed to treat prostate cancer and other solid tumors.     

一株人胰腺癌细胞系的建立及其特性

人胰腺癌是很难建系的癌细胞之一,特别是从原发瘤建立的细胞系。我们成功地从一个胰腺癌组织建立了一株人胰腺癌细胞系,命名为PC-3。PC-3细胞呈上皮样,贴壁生长,经过四年连续培养,细胞系稳定。通过免疫组化、电镜观察、染色体及DNA含量分析,细胞集落形成及裸鼠移植,生长因子对瘤细胞生长的影响和癌基因的表达证实PC-3细胞系为人胰腺癌细胞系。PC-3细胞系的建立进一步丰富了人胰腺癌细胞库,对深入了解人胰腺癌细胞生物学及分子生物学特性提供了有力的物质基础。     

The human Y chromosome suppresses the tumorigenicity of PC-3, a human prostate cancer cell line, in athymic nude mice

The loss of the Y chromosome is a frequent numerical chromosomal abnormality observed in human prostate cancer. In cancer, loss of specific genetic material frequently accompanies simultaneous inactivation of tumor suppressor genes. It is not known whether the Y chromosome harbors such genes. To address the role of genes on the Y chromosome in human prostate cancer, we transferred a tagged Y chromosome into PC-3, a human prostate cancer cell line lacking a Y chromosome. A human Y chromosome was tagged with the hisD gene and transferred to PC-3 by microcell-mediated chromosome transfer. Tumorigenicity of these PC-3 hybrids was tested in vivo and in vitro, and the results were compared with those of the polymerase chain reaction analyses conducted on the PC-3 hybrids using Y chromosome-specific markers. Among 60 mice injected with 12 different PC-3 hybrids (five mice per hybrid), tumor growth was apparent in only one mouse, whereas tumors grew in all mice injected with the parental PC-3 cells. An in vitro assay showed that the Y chromosome did not suppress anchorage-independent growth of PC-3 cells. We found that addition of the Y chromosome suppressed tumor formation by PC-3 in athymic nude mice, and that this block of tumorigenesis was independent of the in vitro growth properties of the cells. This observation suggests the presence of a gene important for prostate tumorigenesis on the Y chromosome.     

Survivin-siRNA真核重组质粒对前列腺癌移植瘤的抑制作用

 目的：探讨survivin-siRNA真核重组质粒对前列腺癌移植瘤的抑瘤效应,并分析相关机制。方法：体外培养前列腺癌DU145细胞,将细胞注射到裸鼠背部皮下,待移植瘤直径达到8 mm时将瘤无菌取出,分成直径约2 mm的瘤块,手术植入另外的裸鼠皮下,将survivin-siRNA质粒或scrambled siRNA对照质粒电转染进行治疗,描记移植瘤生长曲线,并计算抑制率;通过HE染色、免疫组化染色及TUNEL染色观察survivin-siRNA对移植瘤影响。结果：成功构建裸鼠前列腺癌移植瘤模型。与mock和scrambled siRNA组相比,survivin-siRNA抑瘤率分别为两对照组的61.81%和62.87%;免疫组织化学染色发现：survivin-siRNA质粒明显抑制细胞内survivin表达;TUNEL染色证实治疗组肿瘤细胞凋亡明显增加。结论：重组质粒survivin-siRNA明显抑制DU145细胞移植瘤的生长,抑制内源性 survivin 蛋白的表达并促进细胞凋亡,针对survivin靶点的基因治疗前景广阔。