c-Met-targeted RNA interference inhibits growth and metastasis of glioma U251 cells in vitro

This phase II study was designed to determine the objective response rate and 6-month progression free survival of adult patients with recurrent supratentorial anaplastic glioma when treated with the immune modulator, polyinosinic-polycytidylic acid stabilized with polylysine and carboxymethylcellulose (poly-ICLC). This was an open-labeled, single arm phase II study. Patients were treated with poly-ICLC alone. Patients may have had treatment for no more than two prior relapses. Treatment with poly-ICLC continued until tumor progression. Fifty five patients were enrolled in the study. Ten were ineligible after central review of pathology. Eleven percent of patients (5 of 45) had a radiographic response. Time to progression was known for 39 patients and 6 remain on treatment. The estimated 6-month progression free survival was 24%. The median survival time was 43 weeks. Poly-ICLC was well tolerated, but there was no improvement in 6-month progression free survival compared to historical database nor was there an encouraging objective radiographic response rate. Based on this study, poly-ICLC does not improve 6moPFS in patients with recurrent anaplastic gliomas but may be worth further study in combination with agents such as temozolomide.     

Bcl-xl反义寡核苷酸对裸鼠人鼻咽癌移植瘤抑制作用的研究

目的　探讨bcl xl反义寡核苷酸 (ASODN)对裸鼠人鼻咽癌移植瘤生长和基因表达的抑制作用。方法　建立裸鼠人鼻咽癌模型 ,接种肿瘤细胞后 2 4h之内将bcl xlASODN、序列对照寡核苷酸 (ODN)皮下注射进行治疗 ,观察肿瘤大小变化和组织形态学改变 ,并检测药物治疗后肿瘤细胞中bcl xlmRNA和蛋白表达情况。结果　Bcl xlASODN治疗组裸鼠鼻咽癌的生长受到明显抑制 ,抑瘤率为 41.7% ,其对应的bcl xlmRNA和蛋白水平明显降低 ,与对照组相比 ,差异有显著性 (P <0 .0 1) ,而序列对照ODN治疗组抑瘤率仅为 19.0 % ,差异无显著性 ,对基因的表达亦无明显影响。结论　Bcl xlASODN对裸鼠鼻咽癌移植瘤的生长具有一定的抑制作用 ,为鼻咽癌的治疗提供新的方法。     

cFLIP反义寡核苷酸对人肺腺癌SPCA-1细胞作用的探讨

目的:研究脂质体介导的反义寡核苷酸cFLIP对人肺腺癌细胞系SPCA-1凋亡的影响,探讨反义技术选择性封闭目的基因表达进而发挥抗肿瘤作用的机制.方法:用脂质体lipofectamineTM2000将反义寡核苷酸cFLIP(Lipo-ASODN)和无义寡核苷酸cFLIP(Lipo-NASODN)片断导入人肺腺癌细胞系SPCA-1,通过MTT法分别检测细胞生长情况;应用RT-PCR检测cFLIP基因表达,并用Western Blot检测cFLIP蛋白表达,同时原位末端标记(TUNEL)和流式细胞仪检测细胞凋亡情况.结果:MTT实验显示浓度为0.5μmol/L时Lipo-ASODN组细胞生长曲线逐渐降低,24h细胞抑制率可达71.52%,显著高于Lipo-NASODN组和Liposome对照组(P＜0.01);转染24h后LipoASODN组RT-PCR可见cFLIP基因表达量明显少于对照组(P＜0.01),Western Blot可见cFLIPS蛋白表达呈下降趋势,但cFLIPL变化不明显;TUNEL检测可见反义寡核苷酸组细胞核内出现阳性染色,流式细胞仪检测可见明显凋亡峰,且其作用呈一定的剂量依赖性.结论:反义寡核苷酸转染SPCA-1细胞后,cFLIPL/S基因与蛋白表达显著下调,表明此途径是cFLIPL/S mRNA基因片段诱导肿瘤细胞凋亡的机制之一.     

Inhibition effect of vascular endothelial growth factor antisense oligodeoxynucleotides on C6 glioma

Objective: To explore the probability of vascular endothelial growth factor (VEGF) antisense as a developing new therapeutic strategy for glioma. Methods: VEGF protein expression was detected by S-P immunohistochemical technique.Tumor cell apoptosis was observed by TUNEL method.Results: Compared with control, VEGF protein expression was inhibited by antisense oligodeoxynucleotides in vitro.And the inhibitory effects increased with the increasing concentration. VEGF positive rate was 82.10% in control group, while in 2.5, 5, 10 μmol/L AODN groups, they were 70.00%, 57.85%, 53.20% respectively. No inhibition effect was found in the cell lines treated with missense and senseolig odeoxynucleotides. In vivo, antisense oligodeoxy-nucleotides therapy also inhibited VEGF protein expression and induced the increase of apoptotic tumor cells. However,it has no effect on tumor cell proliferation. Conclusion: It is hopeful that VEGF antisense oligodeoxynucleotides may be a new gene therapy method to glioma through its antiangiogenesis effect by inhibition of VEGF.     

Survivin反义寡核苷酸对人卵巢癌细胞 SKOV3的抑制作用

背景与目的:在大多数肿瘤组织中都发现了 survivin的异常高表达,这说明 survivin在肿瘤发生中具有重要作用.本研究探讨 survivin反义寡核苷酸 (survivin ASODN)对人卵巢癌细胞 SKOV3的抑制作用及其机制.方法:脂质体介导 survivin反义寡核苷酸转染 SKOV3,用 MTT法检测细胞抑制率. Western blot法检测相关基因蛋白表达,应用流式细胞术、梯形 DNA片段分析及 DAPI染色光镜观察细胞凋亡情况.激酶活性检测方法测定半胱氨蛋白水解酶 3( caspase-3)活性的变化.结果:脂质体介导 survivin反义寡核苷酸转染后, SKOV3细胞的生长受到明显抑制, 1 000 ng/ml ASODN转染组的细胞抑制率为( 60.30± 2.95)%,明显高于对照组( P< 0.05).凋亡细胞比率由转染前的 0.65%增加至 32.10% ,SKOV3细胞内 survivin基因蛋白表达下调 26.3%, caspase-3活性为 0.998± 0.001,较对照组显著增高( P< 0.01).结论: Survivin ASODN可通过诱导细胞凋亡抑制细胞生长, 具有明显的抗癌作用.     

Enhancement of radiation-induced apoptosis in raji cell line by Bcl-2 antisense oligodeoxynucleotide

Objective: To investigate whether the Bcl-2 antisense oligonucleotide (ASODN) may enhance radiation-induced apoptosis in Raji cell line. Methods: Cell surviving fraction was determined using the trypan blue dye exclusion assay. The expression level of Bcl-2 protein was assayed by immunofluorescence using fluoresce isothiocyanate label. Apoptosis was detected by Giemsa staining and flow cytomertric cell cycle analysis. Results: It was found that Bcl-2 ASODN combined with radiation had significantly reduced the number of viable cells (P<0.05). There was no difference on cell survival between mismatch Bcl-2 oligodeoxynucleotide/radiation combination and radiation-treated cells alone. Bcl-2 ASODN combined with radiation could significantly inhibit expression of Bcl-2 protein in Raji cells (P<0.05). Cells treated with Bcl-2 ASODN combined with radiation at 72 h displayed classic apoptotic changes. Apoptosis rates of Raji cells treated with Bcl-2 oligodeoxynucleotide/radiation combination and radiation-treated cells alone, respectively. Conclusion: Bcl-2 antisense oligonucleotide can enhance radiation-induced apoptosis in Raji cell line. Foundation item: this work was supported by the grants from The Natural Science Program Foundation of Gaungdong Province(No.021195); and The Guangzhou City Key Foundation of Science and Technology Program (No.2001-Z-037-01). Biography: HE Dong-mei(1968–), female, doctor of medicine, associate professor, Jinan University Medical College, majors in gene diagnosis and therapy of leukemia.     

重组腺病毒介导反义c-myc基因对人肝癌细胞系的治疗作用

目的：探讨重组腺病毒介导反义ｃ－ｍｙｃ基因（Ａｄ－ＡＳｍｙｃ）治疗人肝癌细胞的作用。方法：观察Ａｄ－ＡＳｍｙｃ对人肝癌细胞系的转导效率,通过细胞生长曲线、克隆形成实验、ＤＮＡ片段化分析、ＲＴ－ＰＣＲ、裸鼠皮下移植瘤治疗实验,分析Ａｄ－ＡＳｍｙｃ对人肝癌细胞系Ｂｅｌ－７４０２、ＱＳＧ－７７０１、ＳＭＭＣ－７７２１和ＨＣＣ－９２０４细胞生长和ｃ－ｍｙｃ基因表达及裸鼠肿瘤生长的抑制作用。结果：Ａｄ－ＡＳｍｙｃ可高效转导人肝癌细胞系,抑制细胞生长;转染细胞克隆形成能力降低,克隆成活率为对照组的５３．９％～６９．１％,ｃ－ｍｙｃ基因表达下降;Ａｄ－ＡＳｍｙｃ处理肝癌细胞,ＤＮＡ凝胶电泳出现明显的梯形条带,瘤内注射Ａｄ－ＡＳｍｙｃ可抑制裸鼠皮下移植瘤生长。结论：重组腺病毒介导的反义ｃ－ｍｙｃ基因转移,有可能成为肝癌基因治疗     

基质金属蛋白酶-9反义寡核苷酸对人肺腺癌细胞凋亡及转移能力的影响

背景与目的 基质金属蛋白酶-9（MMP-9）是一个重要的细胞外基质降解酶,与肿瘤的发生发展生长密切相关。本研究初步探讨MMP-9反义寡核苷酸（MMP-9ASODN）对人肺腺癌细胞A549凋亡及转移能力的影响。方法 MTT法检测MMP-9ASODN转染对A549细胞生长的影响;流式细胞术检测MMP-9ASODN对A549细胞周期和凋亡比率的影响;MTT比色法和划痕迁移试验观察MMP-9ASODN对A549细胞体外黏附以及迁移的影响。结果 MMP-9ASODN对A549细胞存活率抑制呈浓度和时间依赖性,MMP-9ASODN浓度为600nmol/L、作用48h时抑制作用最明显;与对照组相比,转染MMP-9ASODN的A549细胞凋亡百分比明显升高（P〈0.01）,而黏附力及迁移细胞数显著降低（P〈0.01）。结论 MMP-9ASODN在体外能够显著降低A549细胞的黏附及迁移能力,有效地抑制肺癌A549细胞的增殖,同时促进其凋亡。     

表皮生长因子受体反义cDNA对C6鼠脑胶质瘤体内治疗的研究

目的研究表皮生长因子受体（ＥＧＦＲ）反义ｃＤＮＡ对Ｃ６鼠脑胶质瘤的体内治疗效果。方法将野生型及已转染ＥＧＦＲ反义ｃＤＮＡ的Ｃ６鼠胶质瘤细胞接种于鼠脑右侧尾状核（对照组８只,转染组６只）,并对鼠脑内已形成的Ｃ６胶质瘤用脂质体包裹的ＥＧＦＲ反义ｃＤＮＡ瘤区原位注射（治疗组９只）。观察各组大鼠的一般情况、生存期、肿瘤病理学和磁共振成像（ＭＲＩ）动态改变,采用Ａｇ－ＮＯＲ计数、ＴＵＮＥＬ法检测肿瘤细胞增殖活性及凋亡。结果对照组８只大鼠平均生存期为１７．３天,转染组６只及治疗组６只大鼠生存期明显延长,除因病理检查人为处死外,无自然死亡,存活期超过２００天。ＭＲＩ检查对照组大鼠脑内有明显瘤灶,转染组大鼠未形成瘤灶,治疗组大鼠脑内瘤灶治疗后消失,均与病理学检查结果一致。而且治疗组大鼠Ｃ６细胞增殖活性降低,大量细胞凋亡,ＥＧＦＲ表达减少。结论ＥＧＦＲ可望成为基因治疗的优选靶基因     

The effect of antisense epidermal growth factor receptor (EGFR) RNA on the proliferation of human glioma cells and induction of cell apoptosis

Malignantgliomaisoneofthemostdevastatingdiseases.Theprognosisofpatientshasnotbeenimprovedevenwhenthecurrentlyavailablec0mbinedtherapiesareused.Astheknowledge0ftumorbi0l0gyandmoleculargeneticshasgreatlyincreasedoverthepastdecades,ithasbeenshownthattumorigenesisbasicallyresultsfromtheactivation0fprotooncogenesandinactivati0n0ftumorsuppressorgenes.Sincegenesencodinggrowthfactorsandtheirreceptorsarecloselyrelatedtooncogenes,muchattentionhasbeenfocusedontheroleofgrowthfactorsandtheirreceptorsinthep…     

端粒酶反义脱氧核苷酸与多糖对HL-60细胞的影响

目的　研究人类端粒酶反义脱氧核苷酸及其与梁金菇多糖协同作用对HL 6 0细胞凋亡及端粒酶活性的影响。方法　端粒酶反义脱氧核苷酸单独或与梁金菇多糖协同处理HL 6 0细胞后 ,分别用涂片法、流式细胞仪法和电镜检测两种药物处理后对细胞凋亡的影响 ,以TRAP Elisa法检测对端粒酶活性的影响。结果　端粒酶反义核酸单独或与梁金菇多糖协同处理HL 6 0均可提高细胞的凋亡率并抑制端粒酶活性 ,两者协同处理效果更显著。结论　端粒酶反义核酸可降低细胞的端粒酶活性并诱导细胞调亡 ,梁金菇多糖则可加强这种作用。     

端粒酶RNA的反义寡核苷酸抑制裸鼠移植瘤生长的研究

背景与目的许多研究已证明:端粒酶的激活在肺癌的发生、发展中具有重要作用,因而成为肺癌基因治疗的重要靶点之一。本研究旨在探讨针对人端粒酶RNA成分的反义寡核苷酸对裸鼠移植瘤的生长抑制作用。方法应用人肺腺癌细胞株A549细胞构建裸鼠皮下移植瘤模型,18只荷瘤裸鼠随机分为反义寡核苷酸组(Antisense Oligodeoxynucleotide Group,Group ASODN)、正义寡核苷酸组(Sense Oligodeoxynucleotide Group,Group SODN)和生理盐水对照组(Normal Saline Group,Group NS),每组6只,瘤体内分别注射反义寡核苷酸/阳离子脂质体复合物、正义寡核苷酸/阳离子脂质体复合物和生理盐水,均为每日1次,共14次,观察移植瘤的生长情况。结果反义寡核苷酸组、正义寡核苷酸组的体积抑瘤率分别是43.94%、6.91%,统计学检验有非常显著性差异(t=6.17,P<0.001)。治疗过程中裸鼠对药物耐受良好,无恶心、呕吐等消化道症状,未见皮下出血,治疗结束时各组裸鼠的体重较治疗开始时略有增加。结论瘤体内注射脂质体包封的端粒酶RNA的反义寡核苷酸能够明显抑制裸鼠体内移植瘤的生长。     

靶向miRNA-214反义核酸对白血病U937细胞的生长抑制作用

 【摘要】　目的　探讨以miRNA-214为靶点的反义核酸对白血病U937细胞的生长抑制作用及可能的作用机制。方法　人工合成miRNA-214的反义核酸序列,硫代修饰,以Lipofectamine 2000为介导转入U937细胞。MTT细胞毒性检测U937细胞的增殖活性,流式细胞术检测细胞的凋亡水平,荧光定量PCR检测miRNA-214的表达水平。结果　MTT检测结果显示,转染反义核酸后24 、48、72 h,U937细胞的增殖活性显著下降（0.812 ±0.001、0.770±0.002、0.541±0.001）,与随机对照组（1.011±0.002、1.112±0.003、1.111±0.003）、空白对照组（1.112±0.001、1.023±0.001、1.101±0.001）相比较差异均有统计学意义（F＝2.782、3.659、2.735,P＝0.021、0.018、0.036）。流式细胞术检测结果表明,在转染反义核酸48 h后细胞的凋亡水平随时间延长而提高（48、72 h分别为15.12±0.02、19.14±0.01）,与随机对照组（2.04±0.02、2.45±0.03）、空白对照组（1.19±0.02、2.02±0.01）相比较差异均有统计学意义（F＝3.683、3.762,P＝0.013、0.015）。荧光定量PCR结果证实,在反义核酸作用后,U937细胞内miRNA-214的相对表达水平明显下降（31.1±0.2）,与随机对照组、空白对照组的25.8±0.1、25.6±0.2相比较,差异均有统计学意义（均P＜0.05）。结论　以miRNA-214为靶点的反义核酸可抑制U937细胞的增殖活性,并明显促进细胞的凋亡。     

Effect of BcL-2 antisense drug with different structure on the biological function of K562 cells

Objective: To study the differences and similarities of the antisense drugs with different structures on the biological functions of K562 cells. Methods: Cytotoxic effects were measured by use of a cell viability assay. Flow cytometric analysis and agarose gel electrophoresis of DNA fragmentation were also performed. The expression level of protein was assayed by immunofluorescence using fluoresce isothiocyanate label. Results: PNA targeting the coding region of the Bcl-2 messenger RNA could effectively inhibit K562 cell viability, down-regulate the synthesis of the Bcl-2 protein and increase cell apoptosis. By 72 h after the Bcl-2 antisense PNA treatment, K562 cells showed more reduction in the level of Bcl-2 protein compared with cells treated with the antisense ODN. After treatment with 10 μmol/L of Bcl-2 antisense PNA or antisense ODN for 72 h, apoptotic rates of K562 cells were 13.15±1.13 and 11.72±1.12, respectively. Furthermore, there was significant difference in the percentage of apoptotic cells between antisense PNA group and antisense ODN group. Conclusion: The results suggest that antisense PNA targeting the coding region of Bcl-2 mRNA has better antisense effects than the antisense oligonucleotides on inducing apoptosis of K562 cells. Foundation item: This work was supported by the Key Foundation of Science & Technology Program of Guangzhou (No.2001-Z-037-01), and the Nature Science Key Foundation of Guangdong Province (No. 021195). Biography: LEI Xiao-yong(1970–), male, associate professor, doctor of medicine, Institute of Pharmacy and Pharmacology, Nanhua University, majors in tumor pharmacology.     

心肌细胞裂解液对鼻咽癌CNE-2细胞株的放射增敏作用及其机制的研究

目的 探讨心肌细胞裂解液对鼻咽癌CNE-2细胞的放射增敏作用和机制。方法 采用超滤离心法获得分子量＞10kD、＜5kD及5～10kD的乳Wistar大鼠心肌细胞裂解液超滤液（CMCLnr）、成年Wistar大鼠心肌细胞裂解液超滤液（CMCLar）、乳Wistar大鼠心肌细胞培养液超滤液（CMCMnr）和20日龄乳Wistar大鼠心肌细胞培养液超滤液（CMCM20dr）。用抑瘤活性实验检测上述滤液（0.3mg／ml）和顺铂（1.26μg／ml DDP）作用鼻咽癌CNE-2细胞株的细胞存活率。用放射增敏实验检测CMCLnr（5～10kD）和拓扑替康（TPT）的放射（RT）增敏效果,单击多靶数学模型进行曲线拟合作图。流式细胞术检测TPT、CMCLnr（5～10kD）、RT单独或联合作用CNE 2细胞后细胞周期分布及凋亡率情况。结果 分子量为5～10kD CMCLnr、CMCLar、CMCMnr和CMCM20dr均较对照组能够显著降低CNE-2细胞的存活率（P＜0.05）,且与DDP组差异无统计学意义。CNE-2细胞RT组的D0值为1.185Gy,Dq值为0.676Gy,N值为3.729,SF2为69％; CMCLnr+RT组的D0值为0.762Gy,Dq值为0.600Gy,N值为6.147,SF2为25％,放射增敏比指标SERD0为1.555,SERDq为1.127,SERSF2为2.760。CMCLnr+RT组的细胞凋亡率为（19.34±0.23）％,均高于TPT+RT组和RT组,差异有统计学意义（P＜0.05）。结论 心肌细胞裂解液可抑制鼻咽癌CNE-2细胞的增殖,并对CNE-2细胞具有较强的放射增敏作用,细胞水平的研究表明其放射增敏的机制可能与诱导S期阻滞及促进凋亡有关。     

携带反义c-myc的重组腺病毒安全性研究

目的　研究携带反义c myc的重组腺病毒 (Ad ASmyc)潜在的副作用 ,评价其安全性 ,为其进一步进入临床试验提供依据。方法　用Ad ASmyc感染HeLa细胞 ,制备细胞提取液后反复两次感染HeLa细胞 ,观察Ad ASmyc的繁殖、扩增 ,以及对HeLa细胞的作用 ,RT PCR检测其DNA的转录 ;确定Ad ASmyc对作为正常细胞的人胚肺二倍体细胞 2BS的感染能力 ,绘制细胞生长曲线 ,观察Ad ASmyc对正常细胞的毒性 ;给Balb/c小鼠腹腔注射重组腺病毒后 ,每日观察一般状况 ,化验肝、肾功能 ,PCR检测Ad ASmyc在重要脏器中的分布 ,显微镜观察重要脏器的病理学变化。结果　Ad ASmyc是一复制缺陷型腺病毒 ,它能高效感染 2BS细胞 ,但并不影响其生长 ,小鼠体内应用后 ,无急性毒性症状发生 ,在肝、肾、胃、脾内可检测到腺病毒的分布。但在注射 10 9pfu第 6天、第 12天的小鼠肝组织内可观察到轻微炎症。结论　Ad ASmyc应用是安全的 ,可以进入临床试验。     

骨桥蛋白反义寡核苷酸抑制胃癌细胞MKN28粘附侵袭的实验研究

目的：骨桥蛋白（Osteopontin,OPN）是一种分泌型、粘附性的糖基化磷蛋白,许多肿瘤在发生发展过程中均伴有OPN的表达,而表达OPN的肿瘤也更易表现出侵袭、转移的倾向。本研究将观察OPN反义寡核苷酸（antisense oligonucleotide,ASODN）抑制高分化人胃癌细胞株MKN28粘附侵袭的作用。方法：用脂质体将骨桥蛋白ASODN转染胃癌细胞MKN28,实验分3组,对照组、随机序列寡核苷酸（random oligonucleotide,rODN）组和ASODN组。通过荧光定量RT—PCR、免疫组化方法、粘附细胞计数法、穿透小室聚碳酸酯膜侵袭实验分别测定骨桥蛋白mRNA和细胞表面骨桥蛋白的蛋白表达及癌细胞粘附力、侵袭力的变化。结果：转染后ASODN组骨桥蛋白mRNA的相对定量比值较对照组显著降低（1．83±0．10m3．32±0．16,P〈0．05）;免疫组化检测骨桥蛋白表达结果显示,转染后荧光强度明显降低,细胞表面骨桥蛋白表达下降（P〈0．01）;转染后ASODN组粘附力和侵袭力均较对照组显著下降（粘附细胞百分数为20．50±4．58vs41．50±8．40,穿透聚碳酸酯膜细胞数为21．80±6．90vs．42．00±9．40,P均小于0．01）。而rODN组上述各指标较对照组无明显变化。结论：骨桥蛋白的表达与粘附侵袭能力密切相关,反义寡核苷酸能有效抑制胃癌细胞株MKN28细胞骨桥蛋白基因的表达,从而抑制蛋白质的合成,降低其粘附侵袭能力。     

MicroRNA-204对胶质瘤细胞U251自噬的影响

目的 探讨microRNA-204(miR-204)对胶质瘤细胞U251自噬的影响。方法 采用体外瞬时转染的方法抑制U251细胞中miR-204,MTT方法检测细胞的增殖情况,免疫荧光检测细胞自噬,Western blot检测自噬相关蛋白LC3、Beclin1和Bcl-2的表达情况。结果 MTT结果显示抑制miR-204明显增加U251细胞的增殖,免疫荧光结果显示抑制miR-204能够减少U251细胞的自噬,Western blot结果显示抑制miR-204能够减少U251细胞内LC3-Ⅱ和Beclin1的表达量,然而Bcl-2的表达却明显增加。结论 miR-204可能通过上调Bcl-2的表达抑制自噬促进胶质瘤生长,提示miR-204可能成为脑胶质瘤潜在治疗靶点。     

半乳糖受体介导的c-myc反义寡核苷酸对人肝癌细胞的靶向投递作用

背景与目的:c-myc反义寡核苷酸(antisenseoligodeoxynucleotide,ASODN)能抑制肝癌细胞的增殖,脂质体和腺病毒介导的c-mycASODN投递虽能显著抑制肝癌细胞的增殖,抑制荷肝癌小鼠肿瘤的生长,但这种投递缺乏靶向性;受体介导的药物投递具有高效性和靶向性的特点,已被用于基因及ASODN的靶向投递。本实验以半乳糖(galactose,Gal)-聚乙烯亚胺(polyethyleneimine,PEI)作为载体,介导c-mycASODN作用于人肝癌细胞Bel-7402,探讨c-mycASODN对Bel-7402细胞的靶向投递作用。方法:用流式细胞仪检测Bel-7402、U937细胞对荧光标记的Gal-PEI-c-myc-ASODN(简称Gal-PEI-ASODN)的摄取率及细胞内平均荧光强度;相差/荧光显微镜观察荧光标记的Gal-PEI-ASODN及c-myc-ASODN进入Bel-7402、U937、Raji细胞的形态;台盼蓝拒染法检测不同浓度Gal-PEI-ASODN对这三种细胞增殖的影响。结果:荧光标记的Gal-PEI-ASODN或ASODN与相应细胞孵育10min到4h,Gal-PEI-ASODN-Bel-7402细胞的荧光摄取率为88.25%～98.66%,细胞内平均荧光强度为38.64%～111.90%,与单纯c-mycASODN-Bel-7402细胞组、Gal-PEI-ASODN-U937细胞组相比,所有时间点的细胞荧光摄取率、胞内平均荧光强度均显著增高,经Poission分布检验,均有显著性差异(P<0.01)。相差/荧光显微镜观察到