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受体介导的c-myc反义核酸抑制肝癌Bel-7402细胞增殖的机制[J]. 肿瘤防治研究, 2006, 33(10): 729-732. DOI: 10.3971/j.issn.1000-8578.873
引用本文: 受体介导的c-myc反义核酸抑制肝癌Bel-7402细胞增殖的机制[J]. 肿瘤防治研究, 2006, 33(10): 729-732. DOI: 10.3971/j.issn.1000-8578.873
Mechanism of c-myc Antisense Oligodeoxynucleotide Mediated by Receptor on the Proliferative Inhibition of Bel-7402 Cells[J]. Cancer Research on Prevention and Treatment, 2006, 33(10): 729-732. DOI: 10.3971/j.issn.1000-8578.873
Citation: Mechanism of c-myc Antisense Oligodeoxynucleotide Mediated by Receptor on the Proliferative Inhibition of Bel-7402 Cells[J]. Cancer Research on Prevention and Treatment, 2006, 33(10): 729-732. DOI: 10.3971/j.issn.1000-8578.873

受体介导的c-myc反义核酸抑制肝癌Bel-7402细胞增殖的机制

Mechanism of c-myc Antisense Oligodeoxynucleotide Mediated by Receptor on the Proliferative Inhibition of Bel-7402 Cells

  • 摘要: 目的探讨半乳糖受体介导的c-myc反义寡核苷酸(antisenseoligodeoxynucleotide,ASODN)抑制肝癌Bel-7402细胞增殖的机制。方法c-mycASODN与半乳糖(galactose,Gal)-聚乙烯亚胺(poly-ethyleneimine,PEI)相作用形成Gal-PEI-ASODN复合物,作用于人肝癌Bel-7402细胞,通过流式细胞仪检测细胞周期、AnnexinV-FITC和碘化丙啶(PropidiumIodide,PI)双染色、DNA电泳实验观察Gal-PEI-ASODN对Bel-7402细胞的作用。结果采用流式细胞仪检测细胞周期,细胞对照组、Gal-PEI对照组、ASODN对照组,细胞增殖指数分别为35.04%、33.95%、32.90%,Gal-PEI-ASODN组细胞增殖指数为23.65%,与细胞对照组相比,sub-G1期+G0/G1期细胞总数从64.03%增加到76.74%,S期+G2/M期的细胞从35.04%减少为23.65%,Gal-PEI-ASODN组细胞增殖指数下降11.39%,差异显著(P<0.01)。采用细胞凋亡检测试剂AnnexinV-FITC/P...

     

    Abstract: Objective To observe the mechanism of c-myc antisense oligodeoxynucleotide mediated by galactose receptor on the proliferative inhibition of hepatocarcinoma Bel-7402 cells. Methods c-myc ASODN mixed with Galactose(Gal)- polyethyleneimine(PEI) reagent forming Gal-PEI-ASODN complex,then incubated with Bel-7402 cells for 48h,using Propidium Iodide(PI) dying,AnnexinV-FITC and PI double staining,DNA gel electrophoresis to detected the proliferative inhibition mechanism of Gal-PEI-ASODN on Bel-7402 cells. Results C...

     

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