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首页> 外文期刊>Cancer and Clinical Oncology >The Methylation Analysis of KLF11 and PCDH9 Genes in Patients with Non-Small Cell Lung Cancer
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The Methylation Analysis of KLF11 and PCDH9 Genes in Patients with Non-Small Cell Lung Cancer

机译：非小细胞肺癌患者KLF11和PCDH9基因的甲基化分析

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Background: Lung cancer is the leading cause of cancer-related deaths worldwide and the 5-year survival rate is still very poor due to the lack of effective tools for early detection. Epigenetics and especially studies on DNA methylation have given important information towards a better achievement of lung cancer pathogenesis in the recent decades. The inactivation of tumor suppressor genes via promoter hypermethylation is an obvious mechanism and is straightly related to carcinogenesis. In this study, we compared the methylation status of KLF11 and PCDH9 genes in non-small cell lung cancer and adjacent normal tissues. Methods: Genomic DNA was extracted from 30 tumor tissues, bisulfite treated and were analyzed in terms of promoter methylation status of KLF11 and PCDH9 genes by high resolution melting method. Statistical analysis was carried out by chi-square test. Results: No significant difference in methylation level at the PCDH9 promoter region in NSCLC tumors compared with non-tumor tissues was observed (P = 0.3132, chi-square test). In contrast, the difference in methylation levels between normal and tumor tissue samples for the promoter of the KLF11 gene was quite significant (P = 0.0001). Conclusions: Promoter methylation of KLF11 gene is an important mechanism in the development of NSCLC, therefore, it could be used as one of the potential therapeutic goals for molecular targeted therapy and epigenetic treatment. The role of the PCDH9 gene in the development of lung cancer is complex and requires more research and a larger statistical population.
机译：背景：肺癌是世界范围内与癌症相关的死亡的主要原因，由于缺乏有效的早期检测工具，其5年生存率仍然很低。近几十年来，表观遗传学，尤其是对DNA甲基化的研究，为更好地实现肺癌发病机理提供了重要信息。通过启动子高甲基化使肿瘤抑制基因失活是一个明显的机制，并且与致癌作用直接相关。在这项研究中，我们比较了非小细胞肺癌和邻近正常组织中KLF11和PCDH9基因的甲基化状态。方法：从30个肿瘤组织中提取基因组DNA，用亚硫酸氢盐处理，并通过高分辨率熔解法分析KLF11和PCDH9基因的启动子甲基化状态。通过卡方检验进行统计分析。结果：与非肿瘤组织相比，NSCLC肿瘤中PCDH9启动子区域的甲基化水平没有显着差异（P = 0.3132，卡方检验）。相反，正常和肿瘤组织样品中KLF11基因启动子的甲基化水平差异非常显着（P = 0.0001）。结论：KLF1​​1基因启动子甲基化是NSCLC发展的重要机制，因此可作为分子靶向治疗和表观遗传治疗的潜在治疗目标之一。 PCDH9基因在肺癌发生中的作用是复杂的，需要更多的研究和更大的统计人群。

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