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VEGF反义寡核苷酸对Lewis肺癌细胞的抑制作用 被引量:1

Inhibitory effect of VEGF antisense oligonucleotides on synthesis of VEGF by Lewis lung cancer cells
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摘要 目的:探讨血管内皮生长因子(vascularendothelialgrowthfactor,VEGF)反义寡核苷酸对C57BL/6小鼠肺癌细胞的抑制作用。方法:制作C57BL/6小鼠皮下肺癌模型40只,分为VEGF反义寡核苷酸(ASODN)治疗组、VEGF正义寡核苷酸(SODN)治疗组、VEGF错义寡核苷酸(MODN)治疗组及对照组。接种Lewis肺癌细胞后24h内,用ASODN、SODN及MODN皮下注射进行治疗,对照组只注射生理盐水,观察小鼠肿瘤的生长情况以及组织形态学改变,标本常规石蜡切片,H-E染色,用免疫组化方法检测VEGF蛋白表达。结果:对照组、ASODN组、SODN组、MODN组平均瘤重分别为(7.33±0.71)g、(4.56±0.38)g、(7.59±0.32)g和(7.62±0.39)g,ASODN组、SODN组、MODN组抑瘤率分别为43.8%、5.5%、3.1%。光镜下观察,VEGF-ASODN能明显抑制肿瘤细胞生长,降低增殖活性。免疫组化结果表明,ASODN组VEGF的表达水平明显低于SODN组、MODN组及对照组(P<0.05)。CD34免疫组化结果表明,ASODN组MVD为8.25±2.12,与对照组(14.78±3.51)、SODN组(13.71±3.62)及MODN组(12.81±2.56)比较,ASODN组MVD明显减少(P<0.01)。结论:原位注射VEGF反义寡核苷酸能抑制小鼠肺癌生长。 Objective : To study the inhibitory effect of VEGF antisense oligonucleotides (ASODN) on growth of Lewis lung cancer in C57BL/6 mice. Methods: Lewis lung cancer cells were cultured and implanted subcutaneously into 40 C57BL/6 mice, which were then divided into 4 groups: VEGF-ASODN treatment group, VEGF-SODN treatment group, BEGF-MODN treatment,and control group (normal saline). Mice in different groups were treated 24 hours after cell inoculation. The weight and volume of subcutaneous tumors was measured and the morphological changes of tumor cells was observed under microscope. VEGF protein and microvessel density were examined by immunohistochemistry. Partial tumor tissues were kept in liguid nitrogon. Results: The average tumor weights of the control, VEGF-ASODN, VEGF-SODN and VEGF-MODN groups were (7.33±0.71 )g, (4.56±0.38) g, (7.59±0.32) g, and(7.62±0.39) g, respectively. The inhibition rates of tumor growth in VEGF-ASODN, VEGF-SODN and VEGF-MODN group were 43.8% , 5.5% and 3.1% , respectively. VEGF-ASPODN obviously inhibited the tumor cell growth and decelerated the tumor cell proliferation. Immunohistochemistry results showed that the expression of VEGF in ASODN group was remarkly lower than those in SODN group, MODN group and control group (P〈0.05). The microvessels density (MVD) in the VEGF-ASODN, control, VEGF-SODN, and VEGF-MODN group were 8.25 ± 2.12, 14.78 ± 3.51, 13.71 ± 3.62, and 12.81 ± 2.56, respectively ,with that of VEGF-ASODN remarkly lower than those of other groups( P〈0.01 ). Conclusion : Lewis lung cancer cells can be inhibited by the VEGF antisense oligonucleotides inoculated into tumor in the C57BL/6 mice.
出处 《中国肿瘤生物治疗杂志》 CAS CSCD 2006年第4期281-285,共5页 Chinese Journal of Cancer Biotherapy
基金 黑龙江省"九五"攻关课题资助项目(GDDC190402)
关键词 反义寡核苷酸 血管内皮生长因子 肺癌 antisense oligonucleotides vascular endothelial growth factor lung cancer
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参考文献9

  • 1Konish T,Huang CL,Adachi M,et al.The K-ras gene regulates vascular endothelial growth factor gene expression in non-small cell lung cancers[J].Int J Oncol,2000,16 (3):501-511.
  • 2Ho SP,Britlon DH,Bao Y,et al.RNA mapping:Selection of potent oligonucleotide sequences for antisense experiments[J].Methods Enzymol,2002,314 (12):168-183.
  • 3Gunningham SP,Currie MJ,Han C,et al.Vascular endothelial growth factor-B and vascular endothelial growth factor-C expression in renal cell carcinomas:Regulation by the von hippel-lindau gene and hypoxia[J].Cancer Res,2001,61 (7):3206-3211.
  • 4Lang S,Hartner A,Sterzel RB,et al.Requirement of cyclin D1 in mesangial cell mitogenesis[J].J Am Soc Nephrol,2000,11(8):1398-1408.
  • 5谷仲平.血管内皮生长因子与肺癌(文献综述)[J].国外医学(外科学分册),2002,29(4):232-234. 被引量:3
  • 6Triantafilou M,Triantafilou K,Fernandez N.Rough and smooth forms of fluorescein-labelled bacterial endotoxin exhibit CD14/LBP dependent and independent binding that is influencedby endotoxin concentration[J].Eur J Biochem,2000,267(8):2218-2226.
  • 7孙玲,邹雄,等.血管内皮生长因子在肿瘤中的表达及其临床意义[J].肿瘤防治杂志,2001,8(2):194-196. 被引量:4
  • 8任正刚,金由辛,薛琼,高冬梅,孙方宪.血管内皮生长因子反义寡核苷酸抑制裸鼠人肝癌模型的作用观察[J].中华医学杂志,1999,79(1):65-66. 被引量:8
  • 9Shi W,Siemann DW.Inhibition of renal cell carcinoma angiogenesis and growth by antisense oligonucleotides targeting vascular endothelial growth factor[J].Br J Cancer,2002,87 (1):119-126.

二级参考文献42

  • 1孙宪,汤钊猷,刘康达,叶胜龙,薛琼.裸鼠人肝癌原位移植转移模型的生长特性及转移潜能[J].中华医学杂志,1995,75(11):673-675. 被引量:19
  • 2金冬雁 黎孟枫(译).黎合酶链式反应体外扩增DNA.分子克隆实验指南(第2版)[M].北京:科学出版社,1992.672-684.
  • 3董凡,肿瘤,1997年,17卷,63页
  • 4孙仿宪,中华医学杂志,1995年,11卷,673页
  • 5金冬雁(译),分子克隆实验指南(第2版),1992年,672页
  • 6Carmeliet P, et al. Nature 2000; 407(6801):249-257.
  • 7Shibuya M. Cell Struct Funct 2001;26(1): 25-35.
  • 8Ferrara N, et al. Biochem Biophys Res Commun 1989; 161(2): 851-858.
  • 9Senger DR, et al. Science 1983; 219(4587):983-985.
  • 10Hyder SM, et al. Cancer Res 1998; 58(3):392-395.

共引文献12

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  • 1许凤娣,金志军.肿瘤的反义核酸治疗[J].国外医学(生理病理科学与临床分册),1995,15(3):149-151. 被引量:8
  • 2沈关心 周汝麟.现代免疫学实验技术[M] 2版[M].武汉:湖北科学技术出版社,2002.398-400.
  • 3司徒镇强 吴军正.细胞培养[M].西安:世界图书版出版公司,2004.78-202.
  • 4Kikuchi Y.The mechanism of cisplatin-resistance in ovarian cancer[J].Hum Cell,2001,14(2):115-133.
  • 5Armstrong DK.Relapsed ovarian cancer:challenges and management strategies for a chronic disease[J].Oncologist,2002,7(suppl5):20-28.
  • 6Notarbartolo M,Cervello M,Dusonchet L,et al.Resistance to diverse apoptotic triggers in multidrug resistant HL60 cells and its possible relationship to the expression of P-glycoprotein,Fas and of the novel anti-apoptosis factors IAP(inhibitory of apoptosis proteins)[J].Cancer Lett,2002,180(1):91-101.
  • 7Nieminen AI,Partanen JI,Hau A,et al.c-myc primed mitochondria determine cellular sensitivity to TRAIL-induced apoptosis[J].EMBO J,2007,26(4):1055-1067.
  • 8Sinha BK,Yamazaki H,Eliot HM,et al.Relationships between proto-oncogene expression and apoptosis induced by anti-cancer drugs in human prostate tumor cells[J].Biochim Biophys Acta,1995,1270(1):12-18.
  • 9Saeki T,Tsuruo T,Sato W,et al.,Drug resistance in chemotherapy for breast cancer[J].Cancer Chemath Pharmacol,2005,56(Suppl 1):84-89.
  • 10He Y,Zhang J,Zhang J,et al.The role of c-myc in regulating mdrl gene expression in tumor cell line KB[J].Chin Med J(Engl),2000,113(9):848-851.

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