【摘要】 目的:探讨重组改构人肿瘤坏死因子-α（rmhTNF-α）抑制人胃癌细胞增殖的作用机制。方法:将不同浓度(0、50、100、200 U·ml^-1)的rmhTNF-α作用于人胃癌细胞系MKN45（干预组）,采用增殖/毒性检测试剂（CCK-8）测定细胞抑制率,实时荧光定量PCR测定Δ133p53、cjun、cfos mRNA表达变化。结果:细胞抑制率干预组高于对照组(rmhTNF-α0 U·ml^-1组),且随rmhTNF-α浓度的增加而增高（P<0.05）;Δ133p53mRNA表达干预组较对照组低,且随rmhTNF-α浓度的增加而降低（P<0.05）,cjun、cfos mRNA表达干预组较对照组高,且随rmhTNF-α浓度的增加而增高（均P<0.05）。Pearson相关分析显示,Δ133p53 mRNA与cjun和cfos mRNA的表达呈显著负相关（分别r=-0.954、-0.947,均P<0.01）。结论:rmhTNF-α可能是通过抑制Δ133p53表达并促进cjun、cfos表达而抑制胃癌细胞的增殖,其对Δ133p53的抑制作用可能是cjun、cfos介导的。更多还原

【Abstract】 Objective: To investigate the mechanism of recombinant mutant human tumor necrosis factor-α（rmhTNF-α） inhibit the proliferation of human gastric cancer cell. Methods: Human gastric cancer cell lines MKN45 were treated with different concentrations(0,50,100,200 U·ml^-1) of rmhTNF-α intervention group. The cell inhibition rate was detected by proliferation/toxicity detection kit（CCK-8）,and the expression of Δ133 p53,cjun,cfos mRNA were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction. Results: The cell inhibition rates in the intervention group was higher than that in the control group(rmhTNF-α 0 U·ml^-1 group) and it increased with the increasing of concentration of rmhTNF-α（P < 0. 05）; the expression of Δ133 p53 mRNA in the intervention group was lower than that in the control group and it decreased with the increasing of concentration of rmhTNF-α（P < 0. 05）; the expression of cjun,cfos mRNA in the intervention group were higher than those in the control group and they increased with the increasing of concentration of rmhTNF-α（all P < 0. 05）. Pearson correclation analysis showed the expression was negatively correlated markedly betweenΔ133 p53 mRNA and cjun,cfos mRNA（r =-0. 954,-0. 947,respectivly,all P < 0. 01）. Conclusion: rmhTNF may inhibit Δ133 p53 expression and promote cjun,cfos expression to further inhibit gastric cancer cell proliferation,the inhibitory effect on Δ133 p53 may mediated by cjun and cfos.更多还原