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肺癌组织细胞FHIT 基因启动子甲基化和转录表达[J]. 肿瘤防治研究, 2007, 34(07): 498-500. DOI: 10.3971/j.issn.1000-8578.2226
引用本文: 肺癌组织细胞FHIT 基因启动子甲基化和转录表达[J]. 肿瘤防治研究, 2007, 34(07): 498-500. DOI: 10.3971/j.issn.1000-8578.2226
Transcriptional Expression and Promoter methylation of FHIT gene in Lung Carcinoma Tissues and Cell[J]. Cancer Research on Prevention and Treatment, 2007, 34(07): 498-500. DOI: 10.3971/j.issn.1000-8578.2226
Citation: Transcriptional Expression and Promoter methylation of FHIT gene in Lung Carcinoma Tissues and Cell[J]. Cancer Research on Prevention and Treatment, 2007, 34(07): 498-500. DOI: 10.3971/j.issn.1000-8578.2226

肺癌组织细胞FHIT 基因启动子甲基化和转录表达

Transcriptional Expression and Promoter methylation of FHIT gene in Lung Carcinoma Tissues and Cell

  • 摘要: 目的 探讨FHIT(fragile histidine triad,脆性组氨酸三联体)基因表达水平及其启动子CpG岛甲基化状态与肺癌发生发展的关系。方法 用实时定量PCR检测FHIT mRNA在肺癌组织、肺癌旁组织与去甲基化剂5-氮杂-2'-脱氧胞苷(5-Aza-2'-deoxycytidine、5-Aza—CdR)处理前后A549细胞株中的表达,用甲基化特异性PCR(MS-PCR)检测FHIT启动子CpG岛甲基化状态。结果 FHIT mRNA在肺癌旁组织中全部表达,在肺癌组织中表达缺失率为48.89%(22/45),且表达量低于正常肺组织(t=-15.851,P〈0.001),但在不同年龄和性别、肿瘤大小、恶性程度、肿瘤分类的差异无显著性;FHIT基因启动子在肺癌组织中发生甲基化的频率为40%(18/45)、在癌旁组织中频率8.7%(2/23)(X^2=7.184,P〈0.01),18份启动子区甲基化的肺癌标本中,10份同时伴有mRNA表达缺失。结论 在肺癌组织中,FHIT基因启动子甲基化频率明显升高,其表达缺失或下调,提示FHIT启动子甲基化可在肺癌发生和发展中起一定作用。

     

    Abstract: Objective  To discuss the expression of FHIT (fragile histidine triad) gene in lung carcinoma tissues and cell, its promoter methylation, and analyze the relationship among them. Methods  FHIT mRNA expression was measured by real-time reverse transcription polymerase chain reaction in 45 lung carcinoma, 23 lung side-carcinoma tissues and A549 cell lines. The promoter methylation was determined by methylation-specific PCR(MS-PCR) . Results  FHIT mRNA were all shown in 23 lung side-carcinoma tissues and the loss frequency was 48. 89 %(22/45) in lung carcinoma. The mRNA expression level of FHIT was significantly lower in lung carcinoma than in lung side-carcinoma tissues ( t = - 15. 851 、P <0. 001) . And in the A549 cell lines, the mRNA expression level of FHIT was significantly higher after dealt with 5-Aza-CdR. However, it was not correlated with the clinical data, such as sex, age, pathological type and tumor size ( P > 0. 05) . While the f requency of promoter methylation of Promoter of FHIT gene was 40. 00 % in lung carcinoma and 8. 70 % in lung side-carcinoma tissues (χ2 = 7. 184 、P < 0. 01) .Among 18 patients with aberrant promoter methylation, 10 cases showed the gene inactivation. Conclusion  Frequency of promoter methylation of Promoter of FHIT gene is apparently higher in lung carcinoma tissues than in lung side-carcinoma tissues, and the expression level of FHIT is either lost or lower in lung carcinoma than in lung side-carcinoma tissues. It may contribute to the function in occurrence and development of lung carcinoma.

     

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