张松, 孔维佳, 郭长凯, 王彦君, 韩月臣. 5-杂氮-2’-脱氧胞苷抑制人喉癌裸鼠移植瘤的机制探讨[J]. 中国肿瘤临床, 2005, 32(21): 1212-1215.
引用本文: 张松, 孔维佳, 郭长凯, 王彦君, 韩月臣. 5-杂氮-2’-脱氧胞苷抑制人喉癌裸鼠移植瘤的机制探讨[J]. 中国肿瘤临床, 2005, 32(21): 1212-1215.
Zhang Song, Kong Weijia, Guo Changkai, Wang Yanjun, Han Yuechen. The effect of 5-aza-2-deoxycytidine on Human Laryngeal Carcinoma Xnograft in Nude Mice[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2005, 32(21): 1212-1215.
Citation: Zhang Song, Kong Weijia, Guo Changkai, Wang Yanjun, Han Yuechen. The effect of 5-aza-2-deoxycytidine on Human Laryngeal Carcinoma Xnograft in Nude Mice[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2005, 32(21): 1212-1215.

5-杂氮-2’-脱氧胞苷抑制人喉癌裸鼠移植瘤的机制探讨

The effect of 5-aza-2-deoxycytidine on Human Laryngeal Carcinoma Xnograft in Nude Mice

  • 摘要: 目的: 探讨5-杂氮-2′-脱氧胞苷对Hep-2人喉癌裸鼠移植瘤生长的影响,寻找喉癌治疗的新靶点。 方法: 建立喉癌裸鼠移植瘤模型,用5-杂氮-2′-脱氧胞苷处理裸鼠,观察移植瘤的生长情况并绘制其生长曲线。用RT-PCR和免疫组织化学技术检测死亡相关蛋白激酶(Death-associatedproteinkinaseDAPK)基因mRNA及蛋白表达的变化。 结果: 5-杂氮-2′-脱氧胞苷对人喉癌裸鼠移植瘤处理后用药组和对照组之间裸鼠的体重无明显差异(t=0.011,P0.05),而移植瘤的体积用药组较对照组明显减小,统计学差异有显著性(t=10.11,P0.01)。在喉癌移植瘤组织中,对照组DAPK均不表达,而用药组出现表达。 结论: 5-杂氮-2′-脱氧胞苷在体内能使因甲基化而失活的抑癌基因再转录,诱导其表达,进而抑制喉癌移植瘤的生长。

     

    Abstract: Objective : To explore the effect of 5-Aza-2'-deoxycytidine on the growth of tumor and transcription regulation of DAPK gene in Xenografted of nude mice and to find new target of laryngeal cancer therapy. Methods The model of human laryngeal carcinoma xnograft in nude mice was set up. The growth of those xnografts in nude mice was observed and a growth curve of the xenografted drawn, after treated by 5-Aza-2′-deoxycytidine. RT-PCR and immunohistochemistry were used to determine the expression of DAPK mRNA and protein. Results : No significant difference for body weight of the nude mice was found between the medication group and the controls, after treatment with 5-Aza-2'-deoxycytidine. Volum of human nasopharyngeal carcinoma xnografts in the nude mice of medication group was smaller than those in controls. There was a statistically significant difference between the medication group and the controls, because no expression of DAPK was observed in the control group without treatment of 5-Aza-2ˊ-deoxycytidine. On the contrary, the expression of DAPK was observed in the treatment group. Conclusion : 5-Aza-2'- deoxycytidine may slow down the growth of tumor by reactivating tumor suppressor genes silenced by promoter methylation in vivo.

     

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