腺瘤性结肠息肉病基因启动子 1A 甲基化是否会增加非小细胞肺癌风险？一项荟萃分析。

Does adenomatous polyposis coli gene promoter 1A methylation increase non-small cell lung cancer risk? A meta-analysis.

机构信息

Department Cardiothoracic Surgery, Huaihe Hospital of Henan University, Kaifegn, China.

Department of Clinical Teaching and Research, School of Nursing, Henan University, Kaifegn, China.

出版信息

Thorac Cancer. 2017 Sep;8(5):410-416. doi: 10.1111/1759-7714.12450. Epub 2017 May 12.

DOI:10.1111/1759-7714.12450

PMID:28497891

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5582469/

Abstract

BACKGROUND

The promoter region of the adenomatous polyposis coli (APC) gene is hypermethylated in several types of cancers, including non-small cell lung cancer (NSCLC). The prevalence of methylation in the promoter region of this gene in tumor tissues and autologous controls has not been consistent in previous studies. We evaluated the frequency of APC gene promoter 1A methylation between tumor tissues and autologous controls in NSCLC patients by meta-analysis.

METHODS

Open published studies of APC gene promoter 1A methylation between tumor tissues and autologous samples in NSCLC patients were identified using a systematic search. Odds ratios (OR) and 95% confidence intervals (CI) of APC gene promoter 1A methylation in lung cancer tissues versus autologous controls were calculated. Fourteen studies, involving a total of 1345 patients and 2182 samples, were finally included.

RESULTS

The pooled proportion of APC promoter 1A methylation was 0.62 (95% CI 0.52-072) and 0.34 (95% CI 0.21-0.50) in cancer tissues and autologous controls, respectively. The APC gene promoter 1A methylation rate in cancer tissues was much higher than in autologous controls, with a pooled OR of 3.66 (95% CI 2.12-6.33). A strong and significant correlation of APC gene promoter 1A methylation between tumor tissues and autologous controls was detected (correlation coefficient r = 0.77; P = 0.0013).

CONCLUSION

The proportion of APC promoter 1A methylation in lung cancer tissues was higher than in autologous controls, indicating that promoter 1A methylation of the APC gene may play an important role in NSCLC carcinogenesis.

摘要

背景

腺瘤性结肠息肉病（APC）基因的启动子区域在多种癌症中存在超甲基化，包括非小细胞肺癌（NSCLC）。在之前的研究中，肿瘤组织和自体对照中该基因启动子区域的甲基化发生率并不一致。我们通过荟萃分析评估了 NSCLC 患者肿瘤组织与自体对照中 APC 基因启动子 1A 甲基化的频率。

方法

通过系统搜索，确定了 NSCLC 患者肿瘤组织与自体样本中 APC 基因启动子 1A 甲基化的已发表研究。计算了 APC 基因启动子 1A 在肺癌组织与自体对照中的甲基化比值比（OR）及其 95%置信区间（CI）。最终纳入了 14 项研究，共涉及 1345 例患者和 2182 个样本。

结果

APC 启动子 1A 甲基化的合并比例分别为 0.62（95%CI 0.52-0.72）和 0.34（95%CI 0.21-0.50），在肿瘤组织和自体对照中。肿瘤组织中 APC 基因启动子 1A 甲基化率明显高于自体对照，合并 OR 为 3.66（95%CI 2.12-6.33）。检测到肿瘤组织和自体对照中 APC 基因启动子 1A 甲基化之间存在强而显著的相关性（相关系数 r = 0.77；P = 0.0013）。